Carotid Body
Carotid Body Tumor
Carotid Arteries
Chemoreceptor Cells
Carotid Stenosis
Carotid Artery Diseases
Carotid Sinus
Endarterectomy, Carotid
Carotid Artery, Internal
Carotid Artery, Common
Sodium Cyanide
Carotid Artery, External
Paraganglia, Nonchromaffin
Glossopharyngeal Nerve
Carotid Artery Thrombosis
Carotid Artery Injuries
Carotid Intima-Media Thickness
Aortic Bodies
Respiration
Oxygen
Hypercapnia
Carbon Dioxide
Cats
Tunica Intima
Tunica Media
Domperidone
Pulmonary Ventilation
Carotid Artery, Internal, Dissection
Reflex
Pressoreceptors
Endarterectomy
Sympathectomy
Paraganglioma, Extra-Adrenal
Tyrosine 3-Monooxygenase
Ultrasonography, Doppler, Duplex
Rats, Sprague-Dawley
Cyanides
Ultimobranchial Body
Ganglia, Sensory
Hydrogen Sulfide
Stents
Ischemic Attack, Transient
Cerebral Angiography
Potassium Channels, Tandem Pore Domain
Partial Pressure
Vagotomy
Dopamine
Phrenic Nerve
Rabbits
Angioplasty
Hyperventilation
Stroke
Arteriosclerosis
Respiratory Center
Cerebrovascular Disorders
Paraganglioma
Risk Factors
Magnetic Resonance Angiography
Respiratory Physiological Phenomena
Asphyxia
Electrophysiology
Angioplasty, Balloon
Rats, Wistar
Respiratory Mechanics
Horner Syndrome
Membrane Potentials
Purinergic P2X Receptor Antagonists
Acidosis
Almitrine
Presynaptic action of adenosine on a 4-aminopyridine-sensitive current in the rat carotid body. (1/641)
1. Plasma adenosine concentration increases during hypoxia to a level that excites carotid body chemoreceptors by an undetermined mechanism. We have examined this further by determining the electrophysiological responses to exogenous adenosine of sinus nerve chemoafferents in vitro and of whole-cell currents in isolated type I cells. 2. Steady-state, single-fibre chemoafferent discharge was increased approximately 5-fold above basal levels by 100 microM adenosine. This adenosine-stimulated discharge was reversibly and increasingly reduced by methoxyverapamil (D600, 100 microM), by application of nickel chloride (Ni2+, 2 mM) and by removal of extracellular Ca2+. These effects strongly suggest a presynaptic, excitatory action of adenosine on type I cells of the carotid body. 3. Adenosine decreased whole-cell outward currents at membrane potentials above -40 mV in isolated type I cells recorded during superfusion with bicarbonate-buffered saline solution at 34-36 C. This effect was reversible and concentration dependent with a maximal effect at 10 microM. 4. The degree of current inhibition induced by 10 microM adenosine was voltage independent (45.39 +/- 2. 55 % (mean +/- s.e.m.) between -40 and +30 mV) and largely ( approximately 75 %), but not entirely, Ca2+ independent. 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of the control outward current by 80.60 +/- 3.67 % and abolished the effect of adenosine. 5. Adenosine was without effect upon currents near the resting membrane potential of approximately -55 mV and did not induce depolarization in current-clamp experiments. 6. We conclude that adenosine acts to inhibit a 4-AP-sensitive current in isolated type I cells of the rat carotid body and suggest that this mechanism contributes to the chemoexcitatory effect of adenosine in the whole carotid body. (+info)Trigeminal and carotid body inputs controlling vascular resistance in muscle during post-contraction hyperaemia in cats. (2/641)
1. In anaesthetized cats, the effects of stimulation of the receptors in the nasal mucosa and carotid body chemoreceptors on vascular resistance in hindlimb skeletal muscle were studied to see whether the responses were the same in active as in resting muscle. The measurements of vascular resistance were taken, first, in resting muscle, and second, in the immediate post-contraction hyperaemic phase that followed a 30 s period of isometric contractions. 2. Stimulation of the receptors in the nasal mucosa caused reflex apnoea and vasoconstriction in muscle. The latter response was attenuated when the test was repeated during post-contraction hyperaemia. 3. Stimulations of the carotid bodies were made during a period of apnoea evoked reflexly by electrical stimulation of both superior laryngeal nerves. This apnoea prevented any effects of changes in respiration on the carotid body reflex vascular responses. Stimulation of the carotid bodies evoked hindlimb muscle vasoconstriction. In the post-contraction hyperaemic period, the response was reduced or abolished. A similar attenuation of the reflex vasoconstrictor responses occurred in decentralized muscles stimulated through their motor roots in the cauda equina. 4. Evidence is presented that the attenuation of the vasoconstrictor responses evoked by the two reflexes is a phenomenon localized to the contracting muscles themselves resulting from an interaction between sympathetic neuronal activity and the local production of metabolites. 5. The results are discussed in relation to the metabolic needs of tissues in relation to asphyxial defence mechanisms such as occur in the diving response. (+info)BDNF is a target-derived survival factor for arterial baroreceptor and chemoafferent primary sensory neurons. (3/641)
Brain-derived neurotrophic factor (BDNF) supports survival of 50% of visceral afferent neurons in the nodose/petrosal sensory ganglion complex (NPG; Ernfors et al., 1994a; Jones et al., 1994; Conover et al., 1995; Liu et al., 1995; Erickson et al., 1996), including arterial chemoafferents that innervate the carotid body and are required for development of normal breathing (Erickson et al., 1996). However, the relationship between BDNF dependence of visceral afferents and the location and timing of BDNF expression in visceral tissues is unknown. The present study demonstrates that BDNF mRNA and protein are transiently expressed in NPG targets in the fetal cardiac outflow tract, including baroreceptor regions in the aortic arch, carotid sinus, and right subclavian artery, as well as in the carotid body. The period of BDNF expression corresponds to the onset of sensory innervation and to the time at which fetal NPG neurons are BDNF-dependent in vitro. Moreover, baroreceptor innervation is absent in newborn mice lacking BDNF. In addition to vascular targets, vascular afferents themselves express high levels of BDNF, both during and after the time they are BDNF-dependent. However, endogenous BDNF supports survival of fetal NPG neurons in vitro only under depolarizing conditions. Together, these data indicate two roles for BDNF during vascular afferent pathway development; initially, as a target-derived survival factor, and subsequently, as a signaling molecule produced by the afferents themselves. Furthermore, the fact that BDNF is required for survival of functionally distinct populations of vascular afferents demonstrates that trophic requirements of NPG neurons are not modality-specific but may instead be associated with innervation of particular organ systems. (+info)NADPH oxidase inhibition does not interfere with low PO2 transduction in rat and rabbit CB chemoreceptor cells. (4/641)
The aim of the present work was to elucidate the role of NADPH oxidase in hypoxia sensing and transduction in the carotid body (CB) chemoreceptor cells. We have studied the effects of several inhibitors of NADPH oxidase on the normoxic and hypoxia-induced release of [3H]catecholamines (CA) in an in vitro preparation of intact CB of the rat and rabbit whose CA deposits have been labeled by prior incubation with the natural precursor [3H]tyrosine. It was found that diphenyleneiodonium (DPI; 0.2-25 microM), an inhibitor of NADPH oxidase, caused a dose-dependent release of [3H]CA from normoxic CB chemoreceptor cells. Contrary to hypoxia, DPI-evoked release was only partially Ca2+ dependent. Concentrations of DPI reported to produce full inhibition of NADPH oxidase in the rat CB did not prevent the hypoxic release response in the rat and rabbit CB chemoreceptor cells, as stimulation with hypoxia in the presence of DPI elicited a response equaling the sum of that produced by DPI and hypoxia applied separately. Neopterin (3-300 microM) and phenylarsine oxide (0.5-2 microM), other inhibitors of NADPH oxidase, did not promote release of [3H]CA in normoxic conditions or affect the response elicited by hypoxia. On the basis of effects of neopterin and phenylarsine oxide, it is concluded that NADPH oxidase does not appear to play a role in oxygen sensing or transduction in the rat and rabbit CB chemoreceptor cells in vitro and, in the context of the present study, that DPI effects are not related to NADPH oxidase inhibition. (+info)Enhanced activity of carotid body chemoreceptors in rabbits with heart failure: role of nitric oxide. (5/641)
An enhanced peripheral chemoreflex has been documented in patients with chronic heart failure (CHF). This study aimed to examine the characteristics of carotid body (CB) chemoreceptors in response to isocapnic hypoxia in a rabbit model of pacing-induced CHF and to evaluate the possible role that nitric oxide (NO) plays in the altered characteristics. The chemosensitive characteristics of the CB were evaluated by recording single-unit activity from the carotid sinus nerve in both an intact and a vascularly isolated preparation. It was found that the baseline discharge under normoxia (intact preparation: arterial PO2 90-95 Torr; isolated preparation: PO2 100-110 Torr) and the chemosensitivity in response to graded hypoxia (PO2 40-70 Torr) were enhanced in CHF vs. sham rabbits. These alterations were independent of the CB preparations (intact vs. isolated). NO synthase inhibition by Nomega-nitro-L-arginine increased the baseline discharge and the chemosensitivity in the intact preparation, whereas L-arginine (10(-5) M) inhibited the baseline discharge and the chemosensitivity in the isolated preparation in sham but not in CHF rabbits. S-nitroso-N-acetylpenicillamine, an NO donor, inhibited the baseline discharge and the chemosensitivity in both CB preparations in CHF rabbits but only in the isolated preparation in sham rabbits. The amount of NO produced in vitro by the CB under normoxia was less in CHF rabbits than in sham rabbits (P < 0.05). NO synthase-positive varicosities of nerve fibers within the CB were less in CHF rabbits than in sham rabbits (P < 0.05). These data indicate that an enhanced input from CB occurs in the rabbit model of pacing-induced CHF and that an impairment of NO production may contribute to this alteration. (+info)Nitric oxide inhibits L-type Ca2+ current in glomus cells of the rabbit carotid body via a cGMP-independent mechanism. (6/641)
Previous studies have shown that nitric oxide (NO) inhibits carotid body sensory activity. To begin to understand the cellular mechanisms associated with the actions of NO in the carotid body, we monitored the effects of NO donors on the macroscopic Ca2+ current in glomus cells isolated from rabbit carotid bodies. Experiments were performed on freshly dissociated glomus cells from adult rabbit carotid bodies using the whole cell configuration of the patch-clamp technique. The NO donors sodium nitroprusside (SNP; 600 microM, n = 7) and spermine nitric oxide (SNO; 100 microM, n = 7) inhibited the Ca2+ current in glomus cells in a voltage-independent manner. These effects of NO donors were rapid in onset and peaked within 1 or 2 min. In contrast, the outward K+ current was unaffected by SNP (600 microM, n = 6), indicating that the inhibition by SNP was not a nonspecific membrane effect. 2-(4-carboxyphenyl)-4,4,5, 5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO; 500 microM), an NO scavenger, prevented inhibition of the Ca2+ current by SNP (n = 7), whereas neither superoxide dismutase (SOD; 2,000 U/ml, n = 4), a superoxide scavenger, nor sodium hydrosulfite (SHS; 1 mM, n = 7), a reducing agent, prevented inhibition of the Ca2+ current by SNP. However, SNP inhibition of the Ca2+ current was reversible in the presence of either SOD or SHS. These results suggest that NO itself inhibits Ca2+ current in a reversible manner and that subsequent formation of peroxynitrites results in irreversible inhibition. SNP inhibition of the Ca2+ current was not affected by 30 microM LY 83, 583 (n = 7) nor was it mimicked by 600 microM 8-bromoguanosine 3':5'-cyclic monophosphate (8-Br-cGMP; n = 6), suggesting that the effects of NO on the Ca2+ current are mediated, in part, via a cGMP-independent mechanism. N-ethylmaleimide (NEM; 2.5 mM, n = 6) prevented the inhibition of the Ca2+ current by SNP, indicating that SNP is acting via a modification of sulfhydryl groups on Ca2+ channel proteins. Norepinephrine (NE; 10 microM) further inhibited the Ca2+ current in the presence of NEM (n = 7), implying that NEM did not nonspecifically eliminate Ca2+ current modulation. Nisoldipine, an L-type Ca2+ channel blocker (2 microM, n = 6), prevented the inhibition of Ca2+ current by SNP, whereas omega-conotoxin GVIA, an N-type Ca2+ channel blocker (1 microM, n = 9), did not prevent the inhibition of Ca2+ current by SNP. These results demonstrate that NO inhibits L-type Ca2+ channels in adult rabbit glomus cells, in part, due to a modification of calcium channel proteins. The inhibition might provide one plausible mechanism for efferent inhibition of carotid body activity by NO. (+info)Contribution of baroreceptors and chemoreceptors to ventricular hypertrophy produced by sino-aortic denervation in rats. (7/641)
1. To test whether sino-aortic denervation (SAD)-induced right ventricular hypertrophy (RVH) is a consequence of baroreceptor or chemoreceptor denervation, we compared the effects of aortic denervation (AD), carotid denervation (CD), SAD and a SAD procedure modified to spare the carotid chemoreceptors (mSAD), 6 weeks after denervation surgery in rats. A sham surgery group served as the control. 2. The blood pressure (BP) level was unaffected by AD, CD or SAD, but increased (9 %) following mSAD. The mean heart rate level was not affected. Short-term BP variability was elevated following AD (81 %), SAD (144 %) and mSAD (146 %), but not after CD. Baroreflex heart rate responses to phenylephrine were attenuated in all denervation groups. 3. Significant RVH occurred only following CD and SAD. These procedures also produced high mortality (CD and SAD) and significant increases in right ventricular pressures and haematocrit (CD). 4. Significant left ventricular hypertrophy occurred following CD, SAD and mSAD. Normalized left ventricular weight was significantly correlated with indices of BP variability. 5. These results suggest that SAD-induced RVH is a consequence of chemoreceptor, not baroreceptor, denervation. Our results also demonstrate that a mSAD procedure designed to spare the carotid chemoreceptors produced profound baroreflex dysfunction and significant left, but not right, ventricular hypertrophy. (+info)Contribution of peripheral chemoreception to the depression of the hypoxic ventilatory response during halothane anesthesia in cats. (8/641)
BACKGROUND: The effects of inhalational anesthetics on the hypoxic ventilatory response are complex. This study was designed to determine the contribution of peripheral chemoreception to the depression of hypoxic ventilatory response seen with halothane anesthesia. METHODS: Cats were anesthetized with pentobarbital sodium and alpha-chloralose and artificially ventilated. Respiratory output was evaluated by phasic inspiratory activity of the phrenic nerve. In 12 cats, this activity was measured during inhalation of an hypoxic gas mixture with halothane, 0, 0.1, and 0.8%, with intact or denervated carotid bodies. In 10 cats, a carotid body was isolated from the systemic circulation and perfused with hypoxic Krebs-Ringer solution equilibrated with halothane, 0, 0.1, and 0.8%. RESULTS: The hypoxic ventilatory response was depressed in a dose-dependent manner during halothane anesthesia. In carotid body perfusion studies, the response was significantly depressed only with halothane, 0.80%. CONCLUSION: The hypoxic ventilatory response is depressed by a high dose of halothane through a peripheral effect at the carotid body. (+info)The exact cause of CBTs is not fully understood, but they are thought to be associated with genetic mutations and may be more common in people with a family history of similar tumors. The diagnosis of a carotid body tumor is typically made using imaging tests such as ultrasound, CT or MRI scans, and a biopsy may be performed to confirm the diagnosis.
Treatment for CBTs usually involves surgical removal of the tumor, and in some cases, radiation therapy may also be recommended to reduce the risk of recurrence. The prognosis for patients with CBTs is generally good, but the tumors can recur in some cases.
Preventive measures: There are no specific preventive measures known to prevent carotid body tumors, but early detection and treatment can improve outcomes. Regular neck checks and imaging tests may be recommended for individuals with a family history of these tumors or those who experience symptoms.
Current research: Researchers are working to better understand the causes of CBTs and to develop new treatments that can improve outcomes for patients with these tumors. Studies are ongoing to investigate the genetic mutations that contribute to the development of CBTs and to identify potential targets for therapy. Additionally, researchers are exploring the use of minimally invasive surgical techniques and radiotherapy to treat CBTs.
In summary, carotid body tumors are rare but potentially symptomatic vascular tumors that can be diagnosed and treated with surgery and/or radiation therapy. Early detection and treatment can improve outcomes, and ongoing research is focused on understanding the causes of these tumors and developing new treatments.
There are two main types of carotid stenosis:
1. Internal carotid artery stenosis: This type of stenosis occurs when the internal carotid artery, which supplies blood to the brain, becomes narrowed or blocked.
2. Common carotid artery stenosis: This type of stenosis occurs when the common carotid artery, which supplies blood to the head and neck, becomes narrowed or blocked.
The symptoms of carotid stenosis can vary depending on the severity of the blockage and the extent of the affected area. Some common symptoms include:
* Dizziness or lightheadedness
* Vertigo (a feeling of spinning)
* Blurred vision or double vision
* Memory loss or confusion
* Slurred speech
* Weakness or numbness in the face, arm, or leg on one side of the body
If left untreated, carotid stenosis can lead to a stroke or other serious complications. Treatment options for carotid stenosis include medications to lower cholesterol and blood pressure, as well as surgical procedures such as endarterectomy (removing plaque from the artery) or stenting (placing a small mesh tube in the artery to keep it open).
In conclusion, carotid stenosis is a serious medical condition that can lead to stroke and other complications if left untreated. It is important to seek medical attention if symptoms persist or worsen over time.
The most common carotid artery disease is atherosclerosis, which is the buildup of plaque in the inner lining of the arteries. This buildup can lead to a narrowing or blockage of the arteries, reducing blood flow to the brain and increasing the risk of stroke. Other conditions that can affect the carotid arteries include:
1. Carotid artery stenosis: A narrowing of the carotid arteries caused by atherosclerosis or other factors.
2. Carotid artery dissection: A tear in the inner lining of the arteries that can cause bleeding and blockage.
3. Carotid artery aneurysm: A bulge in the wall of the arteries that can lead to rupture and stroke.
4. Temporal bone fracture: A break in the bones of the skull that can cause damage to the carotid arteries and result in stroke or other complications.
Carotid artery diseases are typically diagnosed using imaging tests such as ultrasound, computed tomography (CT) angiography, or magnetic resonance angiography (MRA). Treatment options for carotid artery diseases depend on the underlying condition and its severity, but may include lifestyle changes, medications, surgery, or endovascular procedures.
Prevention of carotid artery diseases is key to reducing the risk of stroke and other complications. This includes managing risk factors such as high blood pressure, high cholesterol, smoking, and diabetes, as well as maintaining a healthy lifestyle and getting regular check-ups with your doctor.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
Carotid artery thrombosis is often caused by atherosclerosis, which is the buildup of plaque in the arteries that can lead to the formation of blood clots. Other risk factors for carotid artery thrombosis include high blood pressure, smoking, high cholesterol, diabetes, and obesity.
Diagnosis of carotid artery thrombosis typically involves imaging tests such as ultrasound, CT or MRI scans, and Doppler studies to visualize the blood flow in the neck and brain. Treatment options for carotid artery thrombosis include anticoagulation medications to prevent further clotting, medications to dissolve the clot, and surgery to remove the clot or repair the affected artery.
In severe cases, carotid artery thrombosis can lead to stroke or brain damage if not treated promptly. Therefore, it is important to seek medical attention immediately if symptoms persist or worsen over time.
There are several types of carotid artery injuries, including:
1. Carotid artery dissection: This is a tear in the inner lining of the artery that can lead to bleeding and inflammation.
2. Carotid artery thrombosis: This is the formation of a blood clot within the artery that can block blood flow to the brain.
3. Carotid artery occlusion: This is the complete blockage of the artery, which can cause a stroke or transient ischemic attack (TIA).
4. Carotid artery injury due to trauma: This type of injury can occur as a result of a blow to the neck or head.
5. Carotid artery injury due to surgery: This type of injury can occur during surgical procedures that involve the carotid arteries, such as endarterectomy or stenting.
The symptoms of carotid artery injuries can vary depending on the severity of the injury and the location of the damage. Some common symptoms include:
* Sudden weakness or numbness in the face, arm, or leg
* Sudden confusion or trouble speaking
* Sudden vision loss or double vision
* Sudden difficulty walking or maintaining balance
* Sudden severe headache
The diagnosis of carotid artery injuries is typically made using imaging tests such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI). Treatment options for carotid artery injuries depend on the severity and location of the injury, and may include medications, endovascular procedures, or surgery.
Prevention of carotid artery injuries is key to reducing the risk of complications. This can be achieved through:
* Maintaining a healthy lifestyle, including regular exercise and a balanced diet
* Avoiding smoking and limiting alcohol consumption
* Managing underlying medical conditions such as high blood pressure or diabetes
* Properly managing medications that may increase the risk of bleeding or injury
* Using appropriate precautions during surgical procedures, such as using sterile equipment and monitoring for signs of bleeding or injury.
In conclusion, carotid artery injuries can have serious consequences if left untreated. It is important to be aware of the causes, symptoms, diagnosis, and treatment options for these injuries in order to provide appropriate care and prevent complications. Proper precautions during surgical procedures and a healthy lifestyle can also help reduce the risk of carotid artery injuries.
Hypercapnia is a medical condition where there is an excessive amount of carbon dioxide (CO2) in the bloodstream. This can occur due to various reasons such as:
1. Respiratory failure: When the lungs are unable to remove enough CO2 from the body, leading to an accumulation of CO2 in the bloodstream.
2. Lung disease: Certain lung diseases such as chronic obstructive pulmonary disease (COPD) or pneumonia can cause hypercapnia by reducing the ability of the lungs to exchange gases.
3. Medication use: Certain medications, such as anesthetics and sedatives, can slow down breathing and lead to hypercapnia.
The symptoms of hypercapnia can vary depending on the severity of the condition, but may include:
1. Headaches
2. Dizziness
3. Confusion
4. Shortness of breath
5. Fatigue
6. Sleep disturbances
If left untreated, hypercapnia can lead to more severe complications such as:
1. Respiratory acidosis: When the body produces too much acid, leading to a drop in blood pH.
2. Cardiac arrhythmias: Abnormal heart rhythms can occur due to the increased CO2 levels in the bloodstream.
3. Seizures: In severe cases of hypercapnia, seizures can occur due to the changes in brain chemistry caused by the excessive CO2.
Treatment for hypercapnia typically involves addressing the underlying cause and managing symptoms through respiratory support and other therapies as needed. This may include:
1. Oxygen therapy: Administering oxygen through a mask or nasal tubes to help increase oxygen levels in the bloodstream and reduce CO2 levels.
2. Ventilation assistance: Using a machine to assist with breathing, such as a ventilator, to help remove excess CO2 from the lungs.
3. Carbon dioxide removal: Using a device to remove CO2 from the bloodstream, such as a dialysis machine.
4. Medication management: Adjusting medications that may be contributing to hypercapnia, such as anesthetics or sedatives.
5. Respiratory therapy: Providing breathing exercises and other techniques to help improve lung function and reduce symptoms.
It is important to seek medical attention if you suspect you or someone else may have hypercapnia, as early diagnosis and treatment can help prevent complications and improve outcomes.
Hyperoxia can cause damage to the body's tissues and organs, particularly the lungs and brain. In severe cases, hyperoxia can lead to respiratory failure, seizures, and even death.
There are several ways to diagnose hyperoxia, including:
1. Blood tests: These can measure the levels of oxygen in the blood.
2. Arterial blood gas (ABG) analysis: This is a test that measures the amounts of oxygen and carbon dioxide in the blood.
3. Pulse oximetry: This is a non-invasive test that measures the amount of oxygen in the blood by shining a light through the skin.
Treatment for hyperoxia depends on the underlying cause, but may include:
1. Oxygen therapy: This involves administering oxygen to the patient through a mask or nasal tubes.
2. Medications: These may be used to treat any underlying conditions that are causing hyperoxia.
3. Mechanical ventilation: In severe cases, this may be necessary to support the patient's breathing.
In summary, hyperoxia is a condition where there is too much oxygen in the body, and it can cause damage to the body's tissues and organs. Diagnosis is typically made through blood tests or other tests, and treatment may involve oxygen therapy, medications, or mechanical ventilation.
Symptoms of CAID may include sudden weakness or numbness on one side of the body, difficulty speaking, dizziness, and loss of vision in one eye. Diagnosis is typically made through a combination of physical examination, imaging tests such as CT or MRI scans, and Doppler ultrasound.
Treatment for CAID usually involves medications to dissolve blood clots and prevent further complications. In some cases, surgery may be necessary to repair the damaged artery. Preventive measures include avoiding trauma to the neck and head, controlling high blood pressure, and managing underlying medical conditions that increase the risk of CAID.
The carotid arteries are located on either side of the neck and supply oxygen-rich blood to the brain, making them a critical part of the vascular system. Internal dissection of the carotid artery can lead to serious complications if left untreated, so prompt diagnosis and treatment are essential for preventing long-term damage.
Symptoms of an extra-adrenal paraganglioma may include high blood pressure, palpitations, sweating, headaches, and weight loss. The exact cause of this condition is not known, but genetics may play a role in some cases. Treatment options vary depending on the location and size of the tumor, but they often involve surgery to remove the affected tissue.
Example sentence: "The patient experienced a transient ischemic attack, which was caused by a temporary blockage in one of the blood vessels in their brain."
Synonyms: TIA, mini-stroke.
There are several potential causes of hyperventilation, including anxiety, panic attacks, and certain medical conditions such as asthma or chronic obstructive pulmonary disease (COPD). Treatment for hyperventilation typically involves slowing down the breathing rate and restoring the body's natural balance of oxygen and carbon dioxide levels.
Some common signs and symptoms of hyperventilation include:
* Rapid breathing
* Deep breathing
* Dizziness or lightheadedness
* Chest pain or tightness
* Shortness of breath
* Confusion or disorientation
* Nausea or vomiting
If you suspect that someone is experiencing hyperventilation, it is important to seek medical attention immediately. Treatment may involve the following:
1. Oxygen therapy: Providing extra oxygen to help restore normal oxygen levels in the body.
2. Breathing exercises: Teaching the individual deep, slow breathing exercises to help regulate their breathing pattern.
3. Relaxation techniques: Encouraging the individual to relax and reduce stress, which can help slow down their breathing rate.
4. Medications: In severe cases, medications such as sedatives or anti-anxiety drugs may be prescribed to help calm the individual and regulate their breathing.
5. Ventilation support: In severe cases of hyperventilation, mechanical ventilation may be necessary to support the individual's breathing.
It is important to seek medical attention if you or someone you know is experiencing symptoms of hyperventilation, as it can lead to more serious complications such as respiratory failure or cardiac arrest if left untreated.
1. Ischemic stroke: This is the most common type of stroke, accounting for about 87% of all strokes. It occurs when a blood vessel in the brain becomes blocked, reducing blood flow to the brain.
2. Hemorrhagic stroke: This type of stroke occurs when a blood vessel in the brain ruptures, causing bleeding in the brain. High blood pressure, aneurysms, and blood vessel malformations can all cause hemorrhagic strokes.
3. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA is a temporary interruption of blood flow to the brain that lasts for a short period of time, usually less than 24 hours. TIAs are often a warning sign for a future stroke and should be taken seriously.
Stroke can cause a wide range of symptoms depending on the location and severity of the damage to the brain. Some common symptoms include:
* Weakness or numbness in the face, arm, or leg
* Difficulty speaking or understanding speech
* Sudden vision loss or double vision
* Dizziness, loss of balance, or sudden falls
* Severe headache
* Confusion, disorientation, or difficulty with memory
Stroke is a leading cause of long-term disability and can have a significant impact on the quality of life for survivors. However, with prompt medical treatment and rehabilitation, many people are able to recover some or all of their lost functions and lead active lives.
The medical community has made significant progress in understanding stroke and developing effective treatments. Some of the most important advances include:
* Development of clot-busting drugs and mechanical thrombectomy devices to treat ischemic strokes
* Improved imaging techniques, such as CT and MRI scans, to diagnose stroke and determine its cause
* Advances in surgical techniques for hemorrhagic stroke
* Development of new medications to prevent blood clots and reduce the risk of stroke
Despite these advances, stroke remains a significant public health problem. According to the American Heart Association, stroke is the fifth leading cause of death in the United States and the leading cause of long-term disability. In 2017, there were over 795,000 strokes in the United States alone.
There are several risk factors for stroke that can be controlled or modified. These include:
* High blood pressure
* Diabetes mellitus
* High cholesterol levels
* Smoking
* Obesity
* Lack of physical activity
* Poor diet
In addition to these modifiable risk factors, there are also several non-modifiable risk factors for stroke, such as age (stroke risk increases with age), family history of stroke, and previous stroke or transient ischemic attack (TIA).
The medical community has made significant progress in understanding the causes and risk factors for stroke, as well as developing effective treatments and prevention strategies. However, more research is needed to improve outcomes for stroke survivors and reduce the overall burden of this disease.
Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.
There are several types of arteriosclerosis, including:
1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.
Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.
1. Stroke: A stroke occurs when the blood supply to the brain is interrupted, either due to a blockage or a rupture of the blood vessels. This can lead to cell death and permanent brain damage.
2. Cerebral vasospasm: Vasospasm is a temporary constriction of the blood vessels in the brain, which can occur after a subarachnoid hemorrhage (bleeding in the space surrounding the brain).
3. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches. It can lead to recurrent transient ischemic attacks (TIs) or stroke.
4. Cerebral amyloid angiopathy: This is a condition where abnormal protein deposits accumulate in the blood vessels of the brain, leading to inflammation and bleeding.
5. Cavernous malformations: These are abnormal collections of blood vessels in the brain that can cause seizures, headaches, and other symptoms.
6. Carotid artery disease: Atherosclerosis (hardening) of the carotid arteries can lead to a stroke or TIAs.
7. Vertebrobasilar insufficiency: This is a condition where the blood flow to the brain is reduced due to narrowing or blockage of the vertebral and basilar arteries.
8. Temporal lobe dementia: This is a type of dementia that affects the temporal lobe of the brain, leading to memory loss and other cognitive symptoms.
9. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL): This is a rare genetic disorder that affects the blood vessels in the brain, leading to recurrent stroke-like events.
10. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to decreased blood flow to the brain and increased risk of stroke.
It's important to note that this list is not exhaustive and there may be other causes of stroke and TIAs that are not included here. A proper diagnosis can only be made by a qualified medical professional after conducting a thorough examination and reviewing the individual's medical history.
There are several types of apnea that can occur during sleep, including:
1. Obstructive sleep apnea (OSA): This is the most common type of apnea and occurs when the airway is physically blocked by the tongue or other soft tissue in the throat, causing breathing to stop for short periods.
2. Central sleep apnea (CSA): This type of apnea occurs when the brain fails to send the proper signals to the muscles that control breathing, resulting in a pause in breathing.
3. Mixed sleep apnea (MSA): This type of apnea is a combination of OSA and CSA, where both central and obstructive factors contribute to the pauses in breathing.
4. Hypopneic apnea: This type of apnea is characterized by a decrease in breathing, but not a complete stop.
5. Hypercapnic apnea: This type of apnea is caused by an excessive buildup of carbon dioxide in the blood, which can lead to pauses in breathing.
The symptoms of apnea can vary depending on the type and severity of the condition, but may include:
* Pauses in breathing during sleep
* Waking up with a dry mouth or sore throat
* Morning headaches
* Difficulty concentrating or feeling tired during the day
* High blood pressure
* Heart disease
Treatment options for apnea depend on the underlying cause, but may include:
* Lifestyle changes, such as losing weight, avoiding alcohol and sedatives before bedtime, and sleeping on your side
* Oral appliances or devices that advance the position of the lower jaw and tongue
* Continuous positive airway pressure (CPAP) therapy, which involves wearing a mask during sleep to deliver a constant flow of air pressure into the airways
* Bi-level positive airway pressure (BiPAP) therapy, which involves two levels of air pressure: one for inhalation and another for exhalation
* Surgery to remove excess tissue in the throat or correct physical abnormalities that are contributing to the apnea.
Paragangliomas are rare, accounting for less than 1% of all tumors diagnosed in adults. They can occur at any age but are more common in young adults and middle-aged individuals. These tumors are more common in males than females, and their incidence is higher in certain families with inherited syndromes, such as neurofibromatosis type 1 (NF1) or familial paraganglioma.
The symptoms of paraganglioma depend on their location and size. Small tumors may not cause any symptoms, while larger tumors can press on nearby organs and structures, causing a variety of symptoms such as:
* Pain in the abdomen or pelvis
* Swelling or lump in the neck or abdomen
* High blood pressure
* Headaches
* Blurred vision
* Confusion or seizures (in cases of malignant paraganglioma)
Paragangliomas are difficult to diagnose, as they can be mistaken for other conditions such as appendicitis or pancreatitis. Imaging studies such as CT or MRI scans are often used to help identify the location and size of the tumor, while laboratory tests may be used to evaluate hormone levels and other factors that can help differentiate paraganglioma from other conditions.
Treatment for paraganglioma depends on the type, size, and location of the tumor, as well as the patient's overall health status. Small, benign tumors may not require treatment, while larger or malignant tumors may be treated with surgery, chemotherapy, or radiation therapy. In some cases, a combination of these treatments may be used.
The prognosis for paraganglioma is generally good if the tumor is diagnosed and treated early, but it can be poor if the tumor is large or has spread to other parts of the body. With surgical removal of the tumor, the 5-year survival rate is approximately 90% for patients with benign paraganglioma and 30-50% for those with malignant paraganglioma. However, the overall prognosis can vary depending on individual factors such as the size and location of the tumor, the effectiveness of treatment, and the patient's underlying health status.
There are several types of asphyxia, including:
1. Respiratory asphyxia: This occurs when the individual's respiratory system is unable to provide enough oxygen to the body due to obstruction or paralysis of the respiratory muscles.
2. Cardiac asphyxia: This occurs when the heart is unable to pump enough blood to the body, leading to a lack of oxygen and nutrients.
3. Cerebral asphyxia: This occurs when the brain does not receive enough oxygen, leading to impaired consciousness, confusion, seizures, and even death.
4. Hypoxic-ischemic asphyxia: This occurs when there is a lack of oxygen and blood flow to the body's tissues, leading to tissue damage and cell death.
Asphyxia can cause a range of symptoms depending on its severity and duration, including:
1. Difficulty breathing or shortness of breath
2. Confusion, disorientation, or loss of consciousness
3. Slurred speech or inability to speak
4. Seizures or convulsions
5. Pale or blue-tinged skin
6. Low blood pressure
7. Slow heart rate
8. Decreased level of consciousness
Treatment for asphyxia depends on the underlying cause and the severity of the condition. In mild cases, treatment may involve providing oxygen therapy, administering medications to stimulate breathing, or performing other respiratory support measures. In severe cases, hospitalization may be necessary, and treatment may involve mechanical ventilation or other life-saving interventions.
Prevention of asphyxia is essential, and it can be achieved by avoiding situations that can lead to respiratory distress, such as smoking, alcohol consumption, and exposure to toxic substances. It is also important to ensure proper ventilation in enclosed spaces and to use appropriate safety equipment when working with hazardous materials or in confined areas.
In conclusion, asphyxia is a serious condition that can lead to tissue damage and cell death due to a lack of oxygen and blood flow. Prompt recognition and treatment are essential to prevent long-term brain damage and death. Prevention measures include avoiding situations that can lead to respiratory distress and ensuring proper ventilation in enclosed spaces.
The main symptoms of Horner syndrome include:
1. Pain and numbness in the face and arm on one side of the body
2. Weakness or paralysis of the muscles on one side of the face, arm, and hand
3. Difficulty swallowing
4. Reduced sweating on one side of the body
5. Increased heart rate and blood pressure
6. Narrowing of the pupil (anisocoria)
7. Dilation of the unaffected pupil (paralysis of the parasympathetic nervous system)
8. Decreased reflexes
9. Loss of sensation in the skin over the chest and abdomen
10. Pale or clammy skin on one side of the body
The symptoms of Horner syndrome can be caused by a variety of factors, including:
1. Trauma to the thoracolumbar spine
2. Injury or tumor in the brainstem or spinal cord
3. Aneurysm or arteriovenous malformation (AVM) in the neck or chest
4. Multiple sclerosis, amyotrophic lateral sclerosis (ALS), or other neurodegenerative diseases
5. Inflammatory conditions such as sarcoidosis or tuberculosis
6. Infections such as meningitis or abscesses
7. Vasospasm or thrombosis of the blood vessels in the neck or chest.
The diagnosis of Horner syndrome is based on a combination of clinical findings, neuroimaging studies (such as MRI or CT scans), and laboratory tests to rule out other causes of the symptoms. Treatment of the condition depends on the underlying cause and may include surgery, medication, or other interventions. In some cases, Horner syndrome may be a sign of a more serious underlying condition that requires prompt medical attention.
There are several types of acidosis, including:
1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.
The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:
1. Fatigue
2. Weakness
3. Confusion
4. Headaches
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching
If left untreated, acidosis can lead to complications such as:
1. Kidney damage
2. Seizures
3. Coma
4. Heart arrhythmias
5. Respiratory failure
Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:
1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.
In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.
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Expression of the cellular prion protein by mast cells in the human carotid body. | ALZFORUM
Revisions of 'Carotid body tumor' | Case | Radiopaedia.org
Words rhyming with Carotid body
Neurochemical plasticity of the carotid body in hypertension. | Anat Rec (Hoboken);306(9): 2366-2377, 2023 09. | MEDLINE
Fine needle aspiration cytology diagnosis of a case of carotid body tumour | SMJ
Imaging of Head and Neck Glomus Tumors (Paragangliomas): Practice Essentials, Computed Tomography, Magnetic Resonance Imaging
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Carotid artery disease: MedlinePlus Medical Encyclopedia
MeSH Browser
Tumor3
- 6. [Carotid body tumor]. (nih.gov)
- In this article, we reported a case first giving an impression of a thyroid nodule, then suggesting the likelihood of a medullary thyroid carcinoma or intrathyroidal paraganglioma via core needle biopsy, but finally was diagnosed as a carotid body tumor. (archive.org)
- NOTE: Paragangliomas can arise in the jugular fossa / jugular foramen of the temporal bone [glomus jugulare tumors] and in the carotid body [with acronyms that include carotid body tumor, glomus tumor, chemodectomas, and nonchromaffin tumor that are less accurate or obsolete]. (nih.gov)
Arteries10
- The vagus nerve continues by traveling inferiorly within the carotid sheath where it is located posterior and lateral to the internal and common carotid arteries, and medial to the internal jugular vein. (nih.gov)
- The Carotid Artery Disease Program at Tufts Medical Center provides advanced and minimally invasive procedures to treat patients with narrowed carotid arteries due to atherosclerotic, plaque build-up, recurrent stenosis, or fibromuscular dysplasia (FMD). (tuftsmedicalcenter.org)
- The carotid arteries, which pass through the neck and supply blood to the brain, are commonly affected. (nih.gov)
- The carotid arteries should be tested if FMD is found elsewhere in the body since carotid involvement is linked to an increased risk of stroke. (nih.gov)
- Carotid artery disease occurs when the carotid arteries become narrowed or blocked. (medlineplus.gov)
- The carotid arteries provide part of the main blood supply to your brain. (medlineplus.gov)
- Carotid artery disease occurs when fatty material called plaque builds up inside the arteries. (medlineplus.gov)
- Carotid endarterectomy -- This surgery removes the plaque buildup in the carotid arteries. (medlineplus.gov)
- Present on the left and right, the carotid arteries are found in which part of the human body? (triviachamp.com)
- Blood returning to the heart is mostly parallel to the arteries, with subclavian veins, vertebral veins , and (parallel to the carotids) internal and external jugular veins . (factmonster.com)
Tumors16
- About 80% of all glomus tumors are carotid body tumors or glomus jugulare tumors. (medscape.com)
- Haller introduced glomus tumors of the head and neck into the medical record in 1762, when he described a mass at the carotid bifurcation that had a glomus body-like structure. (medscape.com)
- Glomus tumors of the head and neck are associated with 4 primary locations: jugular bulb, middle ear cavity, vagus nerve, and carotid body. (medscape.com)
- 1. [Carotid body tumors: report of ten cases]. (nih.gov)
- 2. Management of carotid body tumors and familial paragangliomas: review of 30 years' experience. (nih.gov)
- 5. Management of Carotid Bifurcation Tumors: 30-Year Experience. (nih.gov)
- 9. Carotid body tumors: challenging complexity of diagnosis and surgical treatment. (nih.gov)
- 10. Carotid body tumors: a review of 30 patients with 46 tumors. (nih.gov)
- 11. [Diagnosis and therapy of carotid body tumors]. (nih.gov)
- 13. Surgical management of carotid body tumors. (nih.gov)
- 14. Surgical treatment of carotid body tumors without embolization. (nih.gov)
- 17. Carotid body tumors. (nih.gov)
- In addition we care for patients with Carotid Body Tumors (paragangiolomas), carotid dissections, and carotid aneurysms. (tuftsmedicalcenter.org)
- Carotid body tumors - can often be peeled off the carotid artery without ever clamping the vessels, though in advanced cases our surgeons may need to replace the diseased segment of artery with a bypass graft. (tuftsmedicalcenter.org)
- In the case of glomus jugulare and carotid body tumors, their clinical presentation and demonstration of avidity on a gallium DOTATATE scan are sufficient. (nih.gov)
- As such, patients who present with glomus jugulare or carotid body tumors will be eligible for enrollment on study based on the clinical/scintigraphic presentation without tissue confirmation. (nih.gov)
Paraganglioma3
- Carotid body tumour (CBT) is a paraganglioma arising from the chief cells of the carotid body, which is situated at the bifurcation of the common carotid artery. (smj.org.sg)
- 18. Outcome of surgical treatment for carotid body paraganglioma. (nih.gov)
- The most common neoplasm was pleomorphic adenoma followed by carotid and vagal paraganglioma 2 . (ispub.com)
Bifurcation2
Vagus nerve4
- When these cells demonstrate neoplasia within the head and neck, they typically present in characteristic locations, including the carotid space, the jugular foramen, the middle ear, and along the course of the vagus nerve. (medscape.com)
- The vagus nerve (cranial nerve [CN] X) is the longest cranial nerve in the body, containing both motor and sensory functions in both the afferent and efferent regards. (nih.gov)
- Because of the wide distribution of the nerve throughout the body, there are several clinical correlations of the vagus nerve. (nih.gov)
- They are most frequently found in the head and neck, mainly associated with the carotid body, vagus nerve, jugulotympanic paraganglia, and occasionaly, the superior-inferior paraganglia. (archive.org)
Chemoreceptor1
- The carotid body (CB), a main peripheral arterial chemoreceptor, has lately been implicated in the pathophysiology of various cardiovascular disorders. (bvsalud.org)
Neck2
- Carotid endarectomy - surgically removing plaque from the artery though a neck incision. (tuftsmedicalcenter.org)
- On each side of the neck there is a major artery-which you feel for when you take your pulse-called the carotid artery (left and right, of course). (factmonster.com)
Artery disease6
- There are many treatment options for Carotid Artery Disease including life style changes, medication, catheter based procedures, and surgery. (tuftsmedicalcenter.org)
- Tufts Medical Center was among the first hospitals in the country to develop a program to treat carotid artery disease. (tuftsmedicalcenter.org)
- While determining the progression of your carotid artery disease, your doctors will also evaluate your risk of related conditions including heart attack and stroke. (tuftsmedicalcenter.org)
- After plaque builds up, the first symptoms of carotid artery disease may be a stroke or a transient ischemic attack (TIA). (medlineplus.gov)
- This sound may be a sign of carotid artery disease. (medlineplus.gov)
- Because there are no symptoms, you may not know you have carotid artery disease until you have a stroke or TIA. (medlineplus.gov)
Angioplasty2
- Carotid angioplasty and stenting - inserting a small mesh tube which is ballooned to open the artery and trap the plaque against the artery wall. (tuftsmedicalcenter.org)
- Carotid angioplasty and stenting -- This procedure opens a blocked artery and places a tiny wire mesh (stent) in the artery to keep it open. (medlineplus.gov)
Tumour1
- 8. Clinical and pathological analysis of malignant carotid body tumour: a report of nine cases. (nih.gov)
Chemodectomas1
- 7. Carotid chemodectomas: long-term results of subadventitial resection with deliberate external carotid resection. (nih.gov)
Sheath1
- The poststyloid compartment contains the carotid sheath with the internal carotid artery, internal jugular vein, the last four cranial nerves and lymph nodes. (ispub.com)
Aortic2
- Well, since most of the body is below the heart, the aorta arches downward (in a part called the aortic arch , of course) almost immediately after it leaves the heart. (factmonster.com)
- Since the aortic arch is more on the left side of the body, the middle branch is the left carotid artery, and the left branch is the left subclavian artery (refer to Figure 12.1). (factmonster.com)
Paragangliomas3
- Paragangliomas arise from paraganglion cells, which serve varied regulatory tasks in the body. (medscape.com)
- 4. A multidisciplinary approach to carotid paragangliomas. (nih.gov)
- 19. Surgical resection of carotid body paragangliomas: 10 years of experience. (nih.gov)
Jugular bulb1
- They arise from glomus cells located within the outermost wall of the jugular bulb or from paraganglionic cells of the carotid body which contains neural elements originating from the neural crest ectoderm. (nih.gov)
Ventilatory1
- In the second group of five animals, neither low- nor high-dose methazolamide changed parameters G, D and A. The observation that even high-dose methazolamide, causing full inhibition of carbonic anhydrase in all body tissues, did not reduce the hypoxic ventilatory response is reminiscent of previous findings by others showing no change in magnitude of the hypoxic response of the in vitro carotid body by this agent. (nih.gov)
Arterial1
- Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats. (nih.gov)
Disease2
- Carotid Artery Occlusive Disease can often be treated with medications, exercise and smoking cessation. (tuftsmedicalcenter.org)
- Since each planet and house are related to particular parts of the body, if the planet or the astrological house has a malefic impact in the horoscope, the particular part of the body may be affected by some disease or handicap. (sunnyray.org)
Glucose3
- Mechanistic and molecular studies in animal models demonstrate that disruptions in circadian rhythms and/or the molecular components of central and peripheral clock proteins profoundly influence glucose and lipid metabolism as well as body adiposity. (nih.gov)
- Epidemiological evidence in humans also suggests that sleep disruption is associated with increased body weight and impaired glucose tolerance. (nih.gov)
- Acute interleukin-6 administration does not impair muscle glucose uptake or whole-body glucose disposal in healthy humans. (duke.edu)
Rats1
- To determine if the carotid body mediated acrolein-induced cardiovascular responses, rats were pretreated with an inhibitor of cystathionine γ-lyase (CSE), an enzyme essential for carotid body signal transduction.Acrolein exposure induced several cardiovascular effects. (nih.gov)
Researcher1
- Researchers, led by British Heart Foundation (BHF)-funded researcher Professor Julian Paton, found that by removing the carotid body connection to the brain in rodents with high blood pressure, blood pressure fell and remained low. (medindia.net)
Vessels2
- When you look at the vessels of the upper body I want you to think about where the blood is coming from, and where it has to go. (factmonster.com)
- We have specialists who regularly perform procedures within blood vessels through an imaging technique known as fluoroscopy, which uses moving X-rays to see inside the body. (chfrichmond.org)
Regulate2
- Normally, the carotid body acts to regulate the amount of oxygen and carbon-dioxide in the blood. (medindia.net)
- Long-chain omega-3 fatty acids regulate bovine whole-body protein metabolism by promoting muscle insulin signalling to the Akt-mTOR-S6K1 pathway and insulin sensitivity. (duke.edu)
Clinical1
- The team's work on carotid body research started in the late 1990's and their recent discovery has since led to a human clinical trial at the Bristol Heart Institute of which the results are expected at the end of the year. (medindia.net)
Plaque1
- The plaque may slowly block or narrow the carotid artery. (medlineplus.gov)
Findings1
- CT imaging is excellent for demonstrating cervical masses along the course of the carotid artery, but findings of skull base soft tissue details can be limited. (medscape.com)
Oxygen1
- The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control. (nih.gov)
Major2
- The carotid body a small nodule (no larger than a rice grain) found on the side of each carotid artery appears to be a major culprit in the development and regulation of high blood pressure. (medindia.net)
- As for the rest of the body, I will get you started with the major pathways here. (factmonster.com)
Organ3
- The nerve travels widely throughout the body affecting several organ systems and regions of the body, such as the tongue, pharynx, heart, and gastrointestinal system. (nih.gov)
- Professor Paton commented: "Despite its small size the carotid body has the highest blood flow of any organ in the body. (medindia.net)
- this is just another example of the body being clever, because a blockage on one side still means that the blood will get to the organ. (factmonster.com)
Cells2
- Expression of the cellular prion protein by mast cells in the human carotid body. (alzforum.org)
- Adenosine is an endogenous nucleoside occurring in all cells of the body. (nih.gov)
External1
- Selective external carotid angiogram reveals a vascular skull base mass. (medscape.com)
Treatment1
- New research indicates that removing one of the tiniest organs in the body has shown to provide effective treatment for high blood pressure. (medindia.net)
Response1
- This response comes about through a nervous connection between the carotid body and the brain. (medindia.net)
Sign1
- How to say carotid body in sign language? (rhymes.com)
Find2
- We couldn't find any rhymes for the word carotid body . (rhymes.com)
- Given the central location of so many structures, one thing you will find throughout the body are examples of collateral circulation (see Figure 12.3). (factmonster.com)
Page1
- This page is about the various possible words that rhymes or sounds like carotid body . (rhymes.com)
Whole body1
- Dietary protein adequacy and lower body versus whole body resistive training in older humans. (duke.edu)