Nitric Oxide Synthase
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Nitric Oxide Donors
Nitric Oxide Synthase Type I
NG-Nitroarginine Methyl Ester
Amino Acid Oxidoreductases
Dose-Response Relationship, Drug
Free Radical Scavengers
Gene Expression Regulation, Enzymologic
Disease Models, Animal
Reactive Oxygen Species
Tumor Necrosis Factor-alpha
Reactive Nitrogen Species
Cyclic GMP-Dependent Protein Kinases
Endothelium-Dependent Relaxing Factors
Analysis of Variance
Electron Spin Resonance Spectroscopy
Persistent Fetal Circulation Syndrome
Reverse Transcriptase Polymerase Chain Reaction
Cyclic Nucleotide Phosphodiesterases, Type 5
Heme Oxygenase (Decyclizing)
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Cationic Amino Acid Transporter 2
Rats, Inbred WKY
Gene Expression Regulation
Anti-Inflammatory Agents, Non-Steroidal
Nitric oxide stimulates the stress-activated protein kinase p38 in rat renal mesangial cells. (1/20782)Nitric oxide (NO) has gained increased attention as a diffusible universal messenger that plays a crucial role in the pathogenesis of inflammatory and autoimmune diseases. Recently, we reported that exogenous NO is able to activate the stress-activated protein kinase (SAPK) cascade in mesangial cells. Here, we demonstrate that exposure of glomerular mesangial cells to compounds releasing NO, including spermine-NO and (Z)-1- (N-methyl-N-[6-(N-methylammoniohexyl)amino]diazen)-1-ium-1,2-diolate (MAHMA-NO), results in an activation of the stress-activated p38-mitogen-activated protein kinase (p38-MAPK) cascade as measured by the phosphorylation of the activator of transcription factor-2 (ATF2) in an immunocomplex kinase assay. Activation of the p38-MAPK cascade by a short stimulation (10 min) with the NO donor MAHMA-NO causes a large increase in ATF2 phosphorylation that is several times greater than that observed after stimulation with interleukin-1beta, a well-known activator of the p38-MAPK pathway. Time course studies reveal that MAHMA-NO causes rapid and maximal activation of p38-MAPK after 10 min of stimulation and that activation declines to basal levels within 60 min. The longer-lived NO donor spermine-NO causes a comparable rapid activation of the p38-MAPK pathway; however, the increased activation state of p38-MAPK was maintained for several hours before control values were reattained after 24 h of stimulation. Furthermore, the NO donors also activated the classical extracellular signal-regulated kinase (ERK) p44-MAPK cascade as shown by phosphorylation of the specific substrate cytosolic phospholipase A2 in an immunocomplex kinase reaction. Both MAHMA-NO and spermine-NO cause a rapid activation of p44-MAPK after 10 min of stimulation. Interestingly, there is a second delayed peak of p44-MAPK activation after 4-24 h of stimulation with NO donors. These results suggest that there is a differential activation pattern for stress-activated and mitogen-activated protein kinases by NO and that the integration of these signals may lead to specific cell responses. (+info)
Relaxin is a potent renal vasodilator in conscious rats. (2/20782)The kidneys and other nonreproductive organs vasodilate during early gestation; however, the "pregnancy hormones" responsible for the profound vasodilation of the renal circulation during pregnancy are unknown. We hypothesized that the ovarian hormone relaxin (RLX) contributes. Therefore, we tested whether the administration of RLX elicits renal vasodilation and hyperfiltration in conscious adult, intact female rats. After several days of treatment with either purified porcine RLX or recombinant human RLX 2 (rhRLX), effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) increased by 20%-40%. Comparable renal vasodilation and hyperfiltration was also observed in ovariectomized rats, suggesting that estrogen and progesterone are unnecessary for the renal response to rhRLX. The nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester completely abrogated the increase in ERPF and GFR elicited by chronic administration of purified porcine RLX. In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment. Short-term infusion of purified porcine RLX to conscious rats over several hours failed to increase ERPF and GFR. Plasma osmolality was consistently reduced by the chronic administration of both RLX preparations. In conclusion, the renal and osmoregulatory effects of chronic RLX administration to conscious rats resemble the physiological changes of pregnancy in several respects: (a) marked increases in ERPF and GFR with a mediatory role for nitric oxide; (b) attenuation of the renal circulatory response to angiotensin II; and (c) reduction in plasma osmolality. (+info)
An antiviral mechanism of nitric oxide: inhibition of a viral protease. (3/20782)Although nitric oxide (NO) kills or inhibits the replication of a variety of intracellular pathogens, the antimicrobial mechanisms of NO are unknown. Here, we identify a viral protease as a target of NO. The life cycle of many viruses depends upon viral proteases that cleave viral polyproteins into individual polypeptides. NO inactivates the Coxsackievirus protease 3C, an enzyme necessary for the replication of Coxsackievirus. NO S-nitrosylates the cysteine residue in the active site of protease 3C, inhibiting protease activity and interrupting the viral life cycle. Substituting a serine residue for the active site cysteine renders protease 3C resistant to NO inhibition. Since cysteine proteases are critical for virulence or replication of many viruses, bacteria, and parasites, S-nitrosylation of pathogen cysteine proteases may be a general mechanism of antimicrobial host defenses. (+info)
Evidence for a vasopressin system in the rat heart. (4/20782)Traditionally, a hypothalamo-neurohypophysial system is thought to be the exclusive source of arginine vasopressin (AVP), a potent antidiuretic, vasoconstricting, and growth-stimulating neuropeptide. We have identified de novo synthesis of AVP in the heart as well as release of the hormone into the cardiac effluents. Specifically, molecular cloning of sequence tags amplified from isolated, buffer-perfused, and pressure-overloaded rat hearts allowed the detection of cardiac AVP mRNA. Subsequent experiments revealed a prominent induction of AVP mRNA (peak at 120 minutes, 59-fold, P<0. 01 versus baseline) and peptide (peak at 120 minutes, 11-fold, P<0. 01 versus baseline) in these isolated hearts. Newly induced vasopressin peptide was localized most prominently to endothelial cells and vascular smooth muscle cells of arterioles and perivascular tissue using immunohistochemistry. In addition to pressure overload, nitric oxide (NO) participated in these alterations, because inhibition of NO synthase by Nomega-nitro-L-arginine methyl ester markedly depressed cardiac AVP mRNA and peptide induction. Immediate cardiac effects related to cardiac AVP induction in isolated, perfused, pressure-overloaded hearts appeared to be coronary vasoconstriction and impaired relaxation. These functional changes were observed in parallel with AVP induction and largely prevented by addition of a V1 receptor blocker (10(-8) mol/L [deamino-Pen1, O-Me-Tyr2, Arg8]-vasopressin) to the perfusion buffer. Even more interesting, pressure-overloaded, isolated hearts released the peptide into the coronary effluents, offering the potential for systemic actions of AVP from cardiac origin. We conclude that the heart, stressed by acute pressure overload or NO, expresses vasopressin in concentrations sufficient to cause local and potentially systemic effects. (+info)
Role of nitric oxide-cGMP pathway in adrenomedullin-induced vasodilation in the rat. (5/20782)We previously reported that adrenomedullin (AM), a potent vasodilator peptide discovered in pheochromocytoma cells, stimulates nitric oxide (NO) release in the rat kidney. To further investigate whether the NO-cGMP pathway is involved in the mechanisms of AM-induced vasodilation, we examined the effects of E-4021, a cGMP-specific phosphodiesterase inhibitor, on AM-induced vasorelaxation in aortic rings and perfused kidneys isolated from Wistar rats. We also measured NO release from the kidneys using a chemiluminescence assay. AM (10(-10) to 10(-7) mol/L) relaxed the aorta precontracted with phenylephrine in a dose-dependent manner. Denudation of endothelium (E) attenuated the vasodilatory action of AM (10(-7) mol/L AM: intact (E+) -25.7+/-5.2% versus denuded (E-) -7. 8+/-0.6%, P<0.05). On the other hand, pretreatment with 10(-8) mol/L E-4021 augmented AM-induced vasorelaxation in the intact aorta (-49. 0+/-7.9%, P<0.05) but not in the denuded one. E-4021 also enhanced acetylcholine (ACh)-induced vasorelaxation in the rat intact aorta (10(-7) mol/L ACh -36.6+/-8.4% versus 10(-8) mol/L E-4021+10(-7) mol/L ACh -62.7+/-3.1%, P<0.05). In perfused kidneys, AM-induced vasorelaxation was also augmented by preincubation with E-4021 (10(-9) mol/L AM -15.4+/-0.6% versus 10(-8) mol/L E-4021+10(-9) mol/L AM -23.6+/-1.2%, P<0.01). AM significantly increased NO release from rat kidneys (DeltaNO: +11.3+/-0.8 fmol. min-1. g-1 kidney at 10(-9) mol/L AM), which was not affected by E-4021. E-4021 enhanced ACh-induced vasorelaxation (10(-9) mol/L ACh -9.7+/-1.7% versus 10(-8) mol/L E-4021+10(-9) mol/L ACh -18.8+/-2.9%, P<0.01) but did not affect ACh-induced NO release from the kidneys. In the aorta and the kidney, 10(-4) mol/L of NG-nitro-L-arginine methyl ester, an NO synthase inhibitor, and 10(-5) mol/L of methylene blue, a guanylate cyclase inhibitor, reduced the vasodilatory effect of AM. These results suggest that the NO-cGMP pathway is involved in the mechanism of AM-induced vasorelaxation, at least in the rat aorta and kidney. (+info)
Overexpression of CuZn superoxide dismutase protects RAW 264.7 macrophages against nitric oxide cytotoxicity. (6/20782)Initiation of nitric oxide (NO.)-mediated apoptotic cell death in RAW 264.7 macrophages is associated with up-regulation of mitochondrial manganese superoxide dismutase (MnSOD; SOD2) and down-regulation of cytosolic copper zinc superoxide dismutase (CuZnSOD; SOD1) at their individual mRNA and protein levels. To evaluate the decreased CuZnSOD expression and the initiation of apoptosis we stably transfected macrophages to overexpress human CuZnSOD. Individual clones revealed a 2-fold increase in CuZnSOD activity. Expression of a functional and thus protective CuZnSOD was verified by attenuated superoxide (O2(.)-)-mediated apoptotic as well as necrotic cell death. In this study we showed that SOD-overexpressing macrophages (R-SOD1-12) were also protected against NO.-initiated programmed cell death. Protection was substantial towards NO. derived from exogenously added NO donors or when NO. was generated by inducible NO synthase activation, and was evident at the level of p53 accumulation, caspase activation and DNA fragmentation. Stimulation of parent and SOD-overexpressing cells with a combination of lipopolysaccharide and murine interferon gamma produced equivalent amounts of nitrite/nitrate, which ruled out attenuated inducible NO. synthase activity during protection. Because protection by a O2(.)--scavenging system during NO. -intoxication implies a role of NO. and O2(.)- in the progression of cell damage, we used uric acid to delineate the role of peroxynitrite during NO.-elicited apoptosis. The peroxynitrite scavenger uric acid left S-nitrosoglutathione or spermine-NO-elicited apoptosis unaltered, blocking only 3-morpholinosydnonimine-mediated cell death. As a result we exclude peroxynitrite from contributing, to any major extent, to NO. -mediated apoptosis. Therefore protection observed with CuZnSOD overexpression is unlikely to stem from interference with peroxynitrite formation and/or action. Unequivocally, the down-regulation of CuZnSOD is associated with NO. cytotoxicity, whereas CuZnSOD overexpression protects macrophages from apoptosis. (+info)
Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells. (7/20782)Under conditions associated with local and systemic inflammation, mesangial cells and invading immune cells are likely to be responsible for the release of large amounts of nitric oxide (NO) in the glomerulus. To further define the mechanisms of NO action in the glomerulus, we attempted to identify genes which are regulated by NO in rat glomerular mesangial cells. We identified vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase (FLT-1) to be under the regulatory control of exogenously applied NO in these cells. Using S-nitroso-glutathione (GSNO) as an NO-donating agent, VEGF expression was strongly induced, whereas expression of its FLT-1 receptor simultaneously decreased. Expressional regulation of VEGF and FLT-1 mRNA was transient and occurred rapidly within 1-3 h after GSNO treatment. Expression of a second VEGF-specific receptor, fetal liver kinase-1 (FLK-1/KDR), could not be detected. The inflammatory cytokine interleukin-1beta mediated a moderate increase in VEGF expression after 24 h and had no influence on FLT-1 expression. In contrast, platelet-derived growth factor-BB and basic fibroblast growth factor had no effect on VEGF expression, but strongly induced FLT-1 mRNA levels. Obviously, there is a differential regulation of VEGF and its receptor FLT-1 by NO, cytokines and growth factors in rat mesangial cells. (+info)
Role of nitric oxide in lipopolysaccharide-induced hepatic injury in D-galactosamine-sensitized mice as an experimental endotoxic shock model. (8/20782)The role of nitric oxide (NO) in lipopolysaccharide (LPS)-induced hepatic injury was studied in D-galactosamine (D-GalN)-sensitized mice. The inducible isoform of NO synthase (iNOS) was immunohistochemically detected on hepatocytes around blood vessels in livers of mice injected with D-GalN and LPS not on hepatocytes in mice injected with D-GalN or LPS alone, although mRNA for iNOS was found in those mice. Nitrotyrosine (NT) was also found in livers of mice injected with D-GalN and LPS. The localization of NT was consistent with that of iNOS, and the time courses of NT and iNOS expression were almost the same. Expression of iNOS and NT was detected exclusively in the hepatic lesions of mice injected with D-GalN and LPS. Anti-tumor necrosis factor alpha neutralizing antibody inhibited iNOS and NT expression and hepatic injury. The results suggested that NO from iNOS may play a role in LPS-induced hepatic injury on D-GalN-sensitized mice as an experimental endotoxic shock model. (+info)
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
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.
The symptoms of PFCS can vary depending on the severity of the condition, but may include:
* Cyanosis (blue discoloration of the skin and mucous membranes)
* Tachypnea (rapid breathing)
* Poor feeding and weight gain
* Fatigue and lethargy
* Low blood pressure
* Abnormal heart rhythms
PFCS is often diagnosed during the newborn period, and treatment may involve a combination of medications, oxygen therapy, and surgical interventions. In some cases, PFCS may be associated with other congenital anomalies, such as heart defects or intestinal atresias.
The prognosis for PFCS varies depending on the severity of the condition and the presence of any additional anomalies. However, early diagnosis and appropriate treatment can improve outcomes and reduce the risk of complications.
Example Sentence: The patient was diagnosed with pulmonary hypertension and began treatment with medication to lower her blood pressure and improve her symptoms.
Word class: Noun phrase / medical condition
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
3. Heart disease
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
In some cases, hyperemia can be a sign of a more serious underlying condition that requires medical attention. For example, if hyperemia is caused by an inflammatory or infectious process, it may lead to tissue damage or organ dysfunction if left untreated.
Hyperemia can occur in various parts of the body, including the skin, muscles, organs, and other tissues. It is often diagnosed through physical examination and imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Treatment for hyperemia depends on its underlying cause, and may include antibiotics, anti-inflammatory medications, or surgery.
In the context of dermatology, hyperemia is often used to describe a condition called erythema, which is characterized by redness and swelling of the skin due to increased blood flow. Erythema can be caused by various factors, such as sun exposure, allergic reactions, or skin infections. Treatment for erythema may include topical medications, oral medications, or other therapies depending on its underlying cause.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Lack of exercise
* High sodium intake
* Low potassium intake
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
Shock refers to a severe and sudden drop in blood pressure, which can lead to inadequate perfusion of vital organs such as the brain, heart, and lungs. There are several types of shock, including hypovolemic shock (caused by bleeding or dehydration), septic shock (caused by an overwhelming bacterial infection), and cardiogenic shock (caused by a heart attack or other cardiac condition).
Septic refers to the presence of bacteria or other microorganisms in the bloodstream, which can cause a range of symptoms including fever, chills, and confusion. Sepsis is a serious and potentially life-threatening condition that can lead to organ failure and death if left untreated.
Septic shock is a specific type of shock that occurs as a result of sepsis, which is the body's systemic inflammatory response to an infection. Septic shock is characterized by severe vasopressor (a medication used to increase blood pressure) and hypotension (low blood pressure), and it can lead to multiple organ failure and death if not treated promptly and effectively.
In summary, shock refers to a drop in blood pressure, while septic refers to the presence of bacteria or other microorganisms in the bloodstream. Septic shock is a specific type of shock that occurs as a result of sepsis, and it can be a life-threatening condition if not treated promptly and effectively.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
Asthma can cause recurring episodes of wheezing, coughing, chest tightness, and shortness of breath. These symptoms occur when the muscles surrounding the airways contract, causing the airways to narrow and swell. This can be triggered by exposure to environmental allergens or irritants such as pollen, dust mites, pet dander, or respiratory infections.
There is no cure for asthma, but it can be managed with medication and lifestyle changes. Treatment typically includes inhaled corticosteroids to reduce inflammation, bronchodilators to open up the airways, and rescue medications to relieve symptoms during an asthma attack.
Asthma is a common condition that affects people of all ages, but it is most commonly diagnosed in children. According to the American Lung Association, more than 25 million Americans have asthma, and it is the third leading cause of hospitalization for children under the age of 18.
While there is no cure for asthma, early diagnosis and proper treatment can help manage symptoms and improve quality of life for those affected by the condition.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
Endotoxemia can occur in individuals who have a severe bacterial infection, such as pneumonia or meningitis, or those who have a prosthetic device or other foreign body that becomes infected with gram-negative bacteria. Treatment of endotoxemia typically involves antibiotics and supportive care to manage symptoms and prevent further complications. In severe cases, medications such as corticosteroids and vasopressors may be used to help reduce inflammation and improve blood flow.
Endotoxemia is a serious medical condition that requires prompt diagnosis and treatment to prevent complications and improve outcomes for patients.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
Exhaled nitric oxide
Nitric oxide synthase
Nitric oxide synthetase
Nitric oxide dioxygenase
Nitric Oxide (journal)
Student Nitric Oxide Explorer
Nitric oxide reductase (menaquinol)
COX-inhibiting nitric oxide donator
Nitric oxide reductase (cytochrome c)
Nitric oxide synthase 2 (inducible)
Biological functions of nitric oxide
Nitric-oxide synthase (NAD(P)H-dependent)
Nitric oxide reductase (NAD(P), nitrous oxide-forming)
Effects of cannabis
Josef von Fodor
William Cruickshank (chemist)
Carbon monoxide poisoning
Frankenstein in popular culture
Health effects of tobacco
Roussin's black salt
Qualitative inorganic analysis
Huntingtin-associated protein 1
Acute tubular necrosis
Local blood flow regulation
Yerevan Thermal Power Plant
Steven R. Tannenbaum
Syntrophin, alpha 1
CDC - NIOSH Pocket Guide to Chemical Hazards - Nitric oxide
Nitric Oxide Nitrogen Mix
What is Fractional Exhaled Nitric Oxide (FeNO) Testing? Fact Sheet | NHLBI, NIH
MedlinePlus - Search Results for: nitric oxide
NITRIC OXIDE - Books - NCBI
Can Nitric Oxide Supplements Help Manage Type 2 Diabetes?
Exhaled nitric oxide measurements in normal and asthmatic children
Grant Abstract: Nitric Oxide Inhibitor and Leihmania Pathogenesis
Nitric oxide - PubMed
NIH VideoCast - The Mitochondrial Nitric Oxide Synthase
nitric oxide - PubChem Substance - NCBI
Nitric Oxide-Related Oxidative Stress and Redox Status in Health and Disease
Another word for NITRIC OXIDE > Synonyms &...
positive regulation of nitric oxide biosynthetic process Gene Ontology Term (GO:0045429)
NITRIC OXIDE AS A NOVEL REGULATOR OF ALTERNATIVE SPLICING
Nitric Oxide | NO | CID 145068 - PubChem
British Library EThOS: The role of nitric oxide in cervical ripening
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- Using Western blotting and immunohistochemistry, the expression and localisation of the enzymes responsible for the production of nitric oxide, inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (bNOS) were determined in the human uterine cervix during pregnancy and parturition. (bl.uk)
- Nitric oxide synthase inhibitor inhibits catecholamines release caused by hypogastric sympathetic nerve stimulation. (aspetjournals.org)
- This was start of a new avenue in my laboratory involving protein nitration, inducible nitric oxide synthase and nitrite production in the context of signaling and gene expression in cancer cells. (eurekaselect.com)
- Studies that used an NO-synthase inhibitor, which prevents the local conversion of precursor molecules as you can find them in our "Nitrix Oxide Booster" Patch to nitric oxide, found that a lack of nitric oxide production inhibits the release of neurotransmitters like serotonin, which makes you happy, and dopamine, which gets you going (Garthwaite. (rawgoods.org)
- By increasing the activity of Nitric Oxide synthase, citrus fruits can help enhance the production of Nitric Oxide in the body. (goodrxmedicine.com)
- Increased inducible nitric oxide synthase expression and oxidation of lung proteins were observed. (cdc.gov)
- Inhibition of inducible nitric oxide synthase with 1400W (1 mg/kg) abrogated the Cl2-induced changes in responsiveness. (cdc.gov)
- Inducible nitric oxide synthase is involved in the induction of changes in responsiveness to methacholine. (cdc.gov)
- Data are presented indicating that in vitro or in vivo exposure to selected occupational dusts, i.e., crystalline silica, organic dust contaminated with endotoxin, or asbestos , results in upregulation of inducible ntric oxide synthase (iNOS) and the production of NO by alveolar macrophages and pulmonary epitelial cells. (cdc.gov)
- A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. (bvsalud.org)
Reactive oxygen species and nitri1
- Furthermore, the efficacy of DFE in inhibiting both reactive oxygen species and nitric oxide were attributed to its phenolic content. (nih.gov)
- Data presented in chapter 5 demonstrate the effect of nitric oxide donors administered in the first trimester of pregnancy on the secretion of MMPs (Matrix Metalloproteinases) -2 and -9 and their tissue inhibitors (TIMPs) in the human cervix. (bl.uk)
- Treatment with the nitric oxide donors spermine nonoate in vitro (non-pregnant cervical biopsies) and isosorbide mononitrate in vivo (pregnant cervical biopsies) had no effect on the secretion of MMPs and TIMPs studied. (bl.uk)
- The mechanism of action of nitric oxide donors in inducing cervical ripening must therefore be attributable to other mechanisms. (bl.uk)
- The mechanism of action of nitric oxide donors was further investigated in chapter 6. (bl.uk)
- In E. coli cells with the combined action of PABA (0.01-5 mM) with nitric oxide donors we observed an inhibition of NO-signaling potency in the SOS (sfiA gene)- and the SoxRS (soxS gene) DNA repair pathway up to 3.5 fold, depending on the dose of PABA. (researchgate.net)
- Coadministration of nitrates or nitric oxide donors is contraindicated due to risk of hypotension. (medscape.com)
Pulsed inhaled nitric oxide1
- The aim of this study was to evaluate the effect of pulsed inhaled nitric oxide (PiNO) during intermittent positive pressure ventilation (IPPV) on arterial oxygenation and right to left vascular shunt in colic horses undergoing abdominal surgery. (slu.se)
Suggest that nitric oxide2
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- Can Nitric Oxide Help with Erectile Dysfunction? (maleextra.com)
- Common drugs for erectile dysfunction treatment including Viagra also work by improving nitric oxide levels in the body. (maleextra.com)
- óxido nítrico)(TT: The year's molecule: 1998 Medicine Nobel Prize) (TA: oxide nitric): An article from: Siempre! (rawgoods.org)
- Sonication induces vasorelaxation almost completely by time-dependent endothelial nitric oxide and prostacyclin release, which appears unrelated to tissue heating or endothelial architectural disruption. (elsevier.com)
- Eventually, even the detrimental effects of smoking are partly mediated via the smoking-impaired reduction of endothelial nitric oxide synthesis (Barua. (rawgoods.org)
- Given this nitric oxide (NO), whereas endothelial derived relationship between endothelial dysfunction and contracting factors are increased 5 . (who.int)
- In addition, RAW 264.7 macrophages and primary human macrophages equipped with NR β-Gal are able to intracellularly convert β-Gal-NONOate into nitric oxide. (au.dk)
- Nitric oxide works as a natural vasodilator and can help protect your heart, increase athletic performance and overall energy levels. (maleextra.com)
- Nitric oxide behaves as a natural vasodilator and expands your arteries for smoother blood flow. (maleextra.com)
- INHALED nitric oxide (NO) is a selective pulmonary vasodilator with therapeutic importance in pulmonary hypertension and respiratory failure. (asahq.org)
- The aim of the studies reported in this thesis was to investigate the potential role of the L-arginine-nitric oxide system in ripening the cervix in humans. (bl.uk)
- Background: Nitric oxide (NO) is a biomediator believed to be synthesized primarily from extracellular arginine. (medscimonit.com)
- Material/Methods: The murine macrophage cell line N-9 was treated with either arginase or arginine deiminase to determine the effect on intracellular and extracellular arginine and nitric oxide production. (medscimonit.com)
- It also showed that L-arginine , a precursor to the production of nitric oxide, plays a vital role in the management of age-related degenerative diseases such as dementia and Alzheimer's disease. (maleextra.com)
- It's crucial to choose Nitric Oxide supplements for ED that contain compounds like L-arginine, L-citrulline, and Pycnogenol, which are known to increase Nitric Oxide synthesis. (goodrxmedicine.com)
- Nitric oxide-releasing silica nanoparticle inhibition of ovarian cancer cell growth. (duke.edu)
- Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP. (bvsalud.org)
- Nitric Oxide Support helps protect muscles from oxidation during intense exercise and delay the onset of muscle fatigue. (pureencapsulations.com.sg)
- to many heme groups-containing proteins, notably hemoglobin, and enzymes, predominantly soluble guanylyl cyclase (sGC), determines both the metabolic fate and the biological activity of NO. Nitric oxide tremendously activates the sGC which catalyses the formation of cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). (hindawi.com)
- NO and your metabolic health: Next to the previously discussed health effects, nitric oxide has also been identified as an important regulator of glucose control. (rawgoods.org)
- You can increase your body's natural production of Nitric Oxide. (goodrxmedicine.com)
- The studies reported in chapter 4 were performed to investigate whether an increase in nitric oxide production occurs in the human cervix in conjunction with cervical ripening. (bl.uk)
- 0.05) and concentration-dependent, reduced nitric oxide production from acterial-lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells was observed with the addition of DFE. (nih.gov)
- Nitric oxide (NO) is an important signaling molecule with multiple pivotal roles in the cardiovascular and neural systems, as well as in inflammatory response. (hindawi.com)
- Nitric oxide (NO) serves either a universal signaling molecule or extremely toxic agent, depending on the dose. (researchgate.net)
Maintaining an erection2
- Biological roles of nitric oxide. (bvsalud.org)
- 2001). There's no doubt about the important role of nitric oxide in the maintenance and function of our immune system. (rawgoods.org)
- Nitric Oxide (NO) plays a crucial role in the relaxation of blood vessels and the regulation of blood flow. (goodrxmedicine.com)
- Objectives: The current study was designed to evaluate protective role of the ethanolic fenugreek seed extract (FSE) and potentiating its effects with nitric oxide (NO) modulators in experimental arthritis and its comparison with the standard drug methotrexate. (who.int)
- Role of nitric oxide in the pathogenesis of dengue. (who.int)
- Ongoing research continues to examine the role of nitric oxide. (medscape.com)
- Role of nitric oxide in the progression of pneumoconiosis. (cdc.gov)
- The measurement of Fractional Exhaled nitric oxide (FENO) was one of two NHANES 2007-8 examination components on respiratory health sponsored by the National Heart, Lung, and Blood Institute of the National Institute of Health. (cdc.gov)
- Nitric Oxide (NO) is a chemical normally produced in the respiratory tract and can be detected in the exhaled breath. (cdc.gov)
- A key regulator of penile erection is Nitric Oxide. (goodrxmedicine.com)
- Energy levels are boosted with the increase in nitric oxide levels. (maleextra.com)
- A lack of L-citrulline can lead to depleted levels of nitric oxide indirectly causing your erections to be soft and inadequate. (maleextra.com)
- NO and your cardiovascular health: Nitric oxide helps you maintain and achieve normal blood pressure levels. (rawgoods.org)
- Garlic is known for its health benefits, and it also contains compounds that can increase Nitric Oxide levels in the body. (goodrxmedicine.com)
- Citrus fruits high in Vitamin C , such as oranges, can increase Nitric Oxide levels in the body. (goodrxmedicine.com)
- Dark chocolate is another food that can help boost Nitric Oxide levels. (goodrxmedicine.com)
- of oxygen (ROS) and nitrog en (RNS). (researchgate.net)
- Some studies have found that nitric oxide helps activate the computational skills of the brain. (maleextra.com)
- Light-Triggered Nitric Oxide Release by a Photosensitizer to Combat Bacterial Biofilm Infections. (bvsalud.org)
- Nitric oxide (NO) has frequently been associated with secondary damage after brain injury. (uni-koeln.de)
- Although the potent antitumor activity of nitric oxide (NO) supports its promise as an antineoplastic agent, effective and selective delivery and action on tumor and not normal cells remains a limiting factor. (duke.edu)
- born forces take perfectly now more in Moon with the read Nitric Oxide: Methods and Protocols Buckingham Palace is this experience to communicate, as and as), with William's desert to the Mount of Olives to increase his sound students to his racism, Princess Alice of Battenberg. (igel-motorsport.de)
- Vasodilators or Nitric Oxide (NO2) producers open up (dilate) blood vessels for up to 24 hours. (supplementscanada.com)
- Nitric oxide has been used by athletes since it was discovered to improve blood flow and overall cardiovascular health. (maleextra.com)
- Nutritionists and doctors both support the fact that patients who suffer from high blood pressure have an impaired ability to utilize nitric oxide's bioavailability. (maleextra.com)
- By widening blood vessels , nitric oxide helps improve blood circulation in the body. (maleextra.com)
- Nitric Oxide supplements can improve blood flow and sexual function. (goodrxmedicine.com)
- The studies reported in chapter 2 were performed in order to compare the effectiveness and side effect profile of the nitric oxide donor (IMN) with the prostaglandin analogue gemeprost. (bl.uk)
- The objective of the nitric oxide data collection was to produce baseline FENO measurements and reference ranges for the U.S. healthy population as well as those with asthma and COPD, and those who are smokers. (cdc.gov)
- During our very first meeting, he not only shared unresolved puzzles in Nitric Oxide (NO) research but also listened to my questions pointing to protein nitration and nitrosylation. (eurekaselect.com)
- The free radical nitric oxide (NO) has emerged in recent years as a fundamental signalling molecule for the maintenance of homeostasis, as well as a potent cytotoxic effector involved in the pathogenesis of a wide range of human diseases. (who.int)
- Without nitric oxide our brains' neurotransmitters system cannot function properly. (rawgoods.org)