Nitroglycerin
Drug Tolerance
Administration, Cutaneous
Vasodilation
Nicorandil
Pentaerythritol Tetranitrate
Dogs
Aldehyde Dehydrogenase
Tilt-Table Test
Spasm
Angina Pectoris
Peripheral Nervous System Agents
Ointments
Vascular Resistance
Nitric Oxide
Hemodynamics
Brachial Artery
Acetylcholine
Endothelium, Vascular
Nitric Oxide Donors
Isosorbide Dinitrate
Diltiazem
Nitrates
Cyclic GMP
Syncope, Vasovagal
Nitroprusside
Papaverine
Guanylate Cyclase
Methylene Blue
Infusions, Intravenous
Double-Blind Method
Coronary Disease
Fissure in Ano
Cyanamide
Radial Artery
Blood Flow Velocity
Coronary Angiography
Vasoconstriction
S-Nitrosothiols
Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation. (1/1442)
BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction. (+info)Coronary vasodilator effects of BNP: mechanisms of action in coronary conductance and resistance arteries. (2/1442)
Brain natriuretic peptide (BNP), a hormone secreted predominantly in ventricular myocytes, may influence coronary vascular tone. We studied the coronary vasodilatory response to BNP under physiological conditions and after preconstriction with endothelin-1 (ET-1) in anesthetized pigs. Average peak-flow velocity (APV) was measured using intracoronary Doppler, and cross-sectional area (CSA) was measured using intravascular ultrasound. Coronary blood flow (CBF) was calculated. Intracoronary BNP induced dose-dependent increases in CSA, APV, and CBF similar in magnitude to those induced by nitroglycerin (NTG). The magnitude of BNP-induced vasodilation was accentuated after preconstriction with ET-1. Pretreatment with either the nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester or the cyclooxygenase inhibitor indomethacin attenuated the coronary vasodilator effect of BNP in resistance arteries without influencing epicardial vasodilation. Pretreatment with the ATP-sensitive potassium-channel blocker glibenclamide enhanced epicardial vasodilation in response to BNP. We conclude that BNP exerts coronary vasodilator effects, predominantly in epicardial conductance vessels. An accentuated vasodilatory response to BNP occurs in ET-1-preconstricted arteries. BNP-induced vasodilation in coronary resistance arteries may be partially mediated via nitric oxide and/or prostaglandin release. (+info)Endothelial function is impaired in fit young adults of low birth weight. (3/1442)
OBJECTIVE: Non-insulin-dependent diabetes, hypertension and ischaemic heart disease, with insulin resistance, are associated with low birth weight (the 'Small Baby Syndrome'). Common to these adult clinical conditions is endothelial dysfunction. We tested the hypothesis that endothelial dysfunction could precede their development in those of low birth weight. METHODS: Endothelial function was measured by ultrasonic 'wall-tracking' of flow-related brachial artery dilatation in fit 19-20 year old subjects randomly selected (blind to the investigators throughout the study) from low (< 2.5 kg) and normal (3.0-3.8 kg) birth weight subjects in the 1975-7 cohort of the Cardiff Births Survey and with no known cause for endothelial dysfunction. RESULTS: Flow-related dilatation was impaired in low birth weight relative to normal birth weight subjects (median 0.04 mm [1.5%] [n = 22] cf. 0.11 mm [4.1%] [n = 17], p < 0.05; 0.04 mm [1.5%] [n = 15] cf. 0.12 mm [4.4%] [n = 12], p < 0.05 after exclusion of inadvertently included ever-smokers). CONCLUSION: The findings suggest that endothelial dysfunction is a consequence of foetal malnutrition, consistent with contributing to the clinical features of the 'Small Baby Syndrome' in later adult life. (+info)Transdermal nitroglycerine enhances spinal sufentanil postoperative analgesia following orthopedic surgery. (4/1442)
BACKGROUND: Sufentanil is a potent but short-acting spinal analgesic used to manage perioperative pain. This study evaluated the influence of transdermal nitroglycerine on the analgesic action of spinal sufentanil in patients undergoing orthopedic surgery. METHODS: Fifty-six patients were randomized to one of four groups. Patients were premedicated with 0.05-0.1 mg/kg intravenous midazolam and received 15 mg bupivacaine plus 2 ml of the test drug intrathecally (saline or 10 microg sufentanil). Twenty to 30 min after the spinal puncture, a transdermal patch of either 5 mg nitroglycerin or placebo was applied. The control group received spinal saline and transdermal placebo. The sufentanil group received spinal sufentanil and transdermal placebo. The nitroglycerin group received spinal saline and transdermal nitroglycerine patch. Finally, the sufentanil-nitroglycerin group received spinal sufentanil and transdermal nitroglycerine. Pain and adverse effects were evaluated using a 10-cm visual analog scale. RESULTS: The time to first rescue analgesic medication was longer for the sufentanil-nitroglycerin group (785+/-483 min) compared with the other groups (P<0.005). The time to first rescue analgesics was also longer for the sufentanil group compared with the control group (P<0.05). The sufentanil-nitroglycerin group group required less rescue analgesics in 24 h compared with the other groups (P<0.02) and had lesser 24-h pain visual analog scale scores compared with the control group (P<0.005), although these scores were similar to the sufentanil and nitroglycerin groups (P>0.05). The incidence of perioperative adverse effects was similar among groups (P>0.05). CONCLUSIONS: Transdermal nitroglycerine alone (5 mg/day), a nitric oxide generator, did not result in postoperative analgesia itself, but it prolonged the analgesic effect of spinal sufentanil (10 microg) and provided 13 h of effective postoperative analgesia after knee surgery. (+info)Effects of nicorandil on aortic input impedance: a comparative study with nitroglycerin. (5/1442)
A study of aortic input impedance was performed to evaluate the effects of nicorandil on the systemic circulation, and the effects were compared with those of nitroglycerin. Sixteen patients with coronary artery disease were divided into 2 age-matched groups. Aortic input impedance was obtained from Fourier analysis of aortic pressure and flow signals at baseline conditions, after intravenous administration of either 4 mg (Group 1) or 8 mg (Group 2) nicorandil, and 20 min after 0.3 mg sublingual nitroglycerin. In Group 1, the first harmonic impedance modulus (Z1, 304+/-140 dyne x s x cm(-5)) and the average of the first to third harmonics (Z1-3, 207+/-99 dyne x s x cm(-5)), indices of wave reflection, significantly decreased (24.4% (p<0.05) and 24.7% (p<0.01), respectively) after nicorandil, and 41.3% (p<0.01) and 33.9% (p<0.01) after nitroglycerin. The effects between the 2 vasodilators were not significantly different. In Group 2, Z1 and Z1-3 (275+/-138 and 196+/-93 dyne x s x cm(-5), respectively) also decreased after administration of nicorandil (28.4% (p<0.01) and 35.9% (p<0.01), respectively), and after administration of nitroglycerin (23.9% (p<0.01) and 28.7% (p<0.01), respectively), without any significant difference between the 2 drugs. Characteristic impedance and total peripheral resistance (R) in both groups remained unchanged except for R after 8 mg nicorandil (from 1830+/-415 to 1433+/-428 dyne x s x cm(-5); p<0.01). Like nitroglycerin, both doses of nicorandil reduced wave reflection. The reduction in R after 8 mg nicorandil is related to decreased tone in the resistance arteries, probably due to potassium channel opener effects. (+info)Does coronary artery morphology predict favorable results of intracoronary thrombolysis in patients with unstable angina pectoris? (6/1442)
The efficacy of intracoronary thrombolysis (ICT) for unstable angina pectoris (UAP) has been limited, despite the similar pathogenesis between UAP and acute myocardial infarction. To ascertain the subset of UAP suitable for ICT, the clinical responses to ICT were assessed in patients with UAP. Eighty-2 patients with medically refractory angina were divided into 2 groups according to the coronary artery morphology of the culprit lesion before ICT: (1) lesions with acute cut off and/or filling defects (AC) and (2) lesions with a tapered shape (TA). The TIMI flow grade was determined from coronary angiograms before and immediately after ICT. The diameter stenosis (%DS) and minimal lumen diameter (MLD) of the culprit lesion were determined using quantitative coronary angiographic analysis before and immediately after ICT. In addition, inhospital cardiac event rates including urgent/emergency coronary angioplasty or bypass surgery, nonfatal myocardial infarction or cardiac death were compared between the 2 groups. Multivariate logistic regression analysis was performed using 13 clinical factors contributing to successful ICT. The results showed that all 3 coronary angiographic parameters (TIMI flow, %DS, and MLD) significantly improved in the AC group (p<0.01, p<0.01 and p<0.05, respectively), whereas none of these parameters improved in the TA group. The inhospital cardiac event rate after ICT was significantly higher in the TA group (76%) than in the AC group (48%; p=0.016). Odds ratio predicting successful ICT was 7.09 (p<0.01) for the AC lesion, and 2.54 (p<0.01) for new angina. In conclusion the AC lesions are more commonly associated with coronary thrombosis that responds to ICT than are the TA lesions. Thus, the coronary angiographic morphology may be an important predictor for a successful ICT in patients with medically refractory UAP. (+info)Nitric-oxide-induced apoptosis in human leukemic lines requires mitochondrial lipid degradation and cytochrome C release. (7/1442)
We have previously shown that nitric oxide (NO) stimulates apoptosis in different human neoplastic lymphoid cell lines through activation of caspases not only via CD95/CD95L interaction, but also independently of such death receptors. Here we investigated mitochondria-dependent mechanisms of NO-induced apoptosis in Jurkat leukemic cells. NO donor glycerol trinitrate (at the concentration, which induces apoptotic cell death) caused (1) a significant decrease in the concentration of cardiolipin, a major mitochondrial lipid; (2) a downregulation in respiratory chain complex activities; (3) a release of the mitochondrial protein cytochrome c into the cytosol; and (4) an activation of caspase-9 and caspase-3. These changes were accompanied by an increase in the number of cells with low mitochondrial transmembrane potential and with a high level of reactive oxygen species production. Higher resistance of the CD95-resistant Jurkat subclone (APO-R) cells to NO-mediated apoptosis correlated with the absence of cytochrome c release and with less alterations in other mitochondrial parameters. An inhibitor of lipid peroxidation, trolox, significantly suppressed NO-mediated apoptosis in APO-S Jurkat cells, whereas bongkrekic acid (BA), which blocks mitochondrial permeability transition, provided only a moderate antiapoptotic effect. Transfection of Jurkat cells with bcl-2 led to a complete block of apoptosis due to the prevention of changes in mitochondrial functions. We suggest that the mitochondrial damage (in particular, cardiolipin degradation and cytochrome c release) induced by NO in human leukemia cells plays a crucial role in the subsequent activation of caspase and apoptosis. (+info)Comparison of atenolol with propranolol in the treatment of angina pectoris with special reference to once daily administration of atenolol. (8/1442)
Fourteen patients with angina pectoris completed a double blind trial of atenolol 25 mg, 50 mg, and 100 mg twice daily and propranolol 80 mg thrice daily. In comparison with placebo, all active treatments significantly reduced anginal attacks, consumption of glyceryl trinitrate, resting and exercise heart rate, resting and exercise systolic blood pressure, and significantly prolonged exercise time. There was no significant difference between the effects of propranolol and atenolol. Nine patients completed a further trial comparing atenolol given once or twice daily. Both regimens were effective and there was no significant difference between the reductions in anginal attacks, glyceryl trinitrate consumption, systolic blood pressure, or heart rate. Twenty-four-hour ambulatory electrocardiograms showed that atenolol consistently reduced heart rate throughout the 24-hour period whether given once or twice daily. Atenolol is a potent antianginal agent which, in most patients, is likely to be effective once daily. (+info)Example sentences:
1. The patient experienced a spasm in their leg while running, causing them to stumble and fall.
2. The doctor diagnosed the patient with muscle spasms caused by dehydration and recommended increased fluids and stretching exercises.
3. The athlete suffered from frequent leg spasms during their training, which affected their performance and required regular massage therapy to relieve the discomfort.
Angina pectoris is a medical condition that is characterized by recurring chest pain or discomfort due to reduced blood flow and oxygen supply to the heart muscle, specifically the myocardium. It is also known as stable angina or effort angina. The symptoms of angina pectoris typically occur during physical activity or emotional stress and are relieved by rest.
The term "angina" comes from the Latin word for "strangulation," which refers to the feeling of tightness or constriction in the chest that is associated with the condition. Angina pectoris can be caused by atherosclerosis, or the buildup of plaque in the coronary arteries, which supply blood to the heart muscle. This buildup can lead to the formation of atherosclerotic plaques that can narrow the coronary arteries and reduce blood flow to the heart muscle, causing chest pain.
There are several types of angina pectoris, including:
1. Stable angina: This is the most common type of angina and is characterized by predictable and reproducible symptoms that occur during specific situations or activities, such as exercise or emotional stress.
2. Unstable angina: This type of angina is characterized by unpredictable and changing symptoms that can occur at rest or with minimal exertion. It is often a sign of a more severe underlying condition, such as a heart attack.
3. Variant angina: This type of angina occurs during physical activity, but the symptoms are not relieved by rest.
4. Prinzmetal's angina: This is a rare type of angina that occurs at rest and is characterized by a feeling of tightness or constriction in the chest.
The diagnosis of angina pectoris is typically made based on a combination of physical examination, medical history, and diagnostic tests such as electrocardiogram (ECG), stress test, and imaging studies. Treatment for angina pectoris usually involves lifestyle modifications, such as regular exercise, a healthy diet, and stress management, as well as medications to relieve symptoms and reduce the risk of complications. In some cases, surgery or other procedures may be necessary to treat the underlying condition causing the angina.
Word Origin: From coronary (pertaining to the crown) + vasospasm (a spasmodic constriction of a blood vessel).
The exact cause of vasovagal syncope is not fully understood, but it is thought to be related to an imbalance in the autonomic nervous system (which controls involuntary functions such as heart rate and blood pressure). It can be triggered by a variety of factors, including:
* Strong emotions such as fear or anxiety
* Pain or discomfort
* Intense physical activity
* Dehydration or low blood sugar
* Certain medications
During a vasovagal syncope episode, the person may experience symptoms such as:
* Dizziness or lightheadedness
* Blurred vision
* Nausea or vomiting
* Sweating
* Feeling of impending doom or loss of control
* Eventually, fainting or falling to the ground
Diagnosis of vasovagal syncope is typically made based on a combination of symptoms and physical examination findings. Tests such as an electrocardiogram (ECG) or blood tests may be ordered to rule out other conditions that may be causing the symptoms. Treatment for vasovagal syncope usually involves addressing any underlying triggers, such as managing stress or avoiding certain stimuli that may cause the episodes. In some cases, medications such as beta blockers or antidepressants may be prescribed to help regulate the heart rate and blood pressure.
Medical Definition of Scorpion Stings:
Scorpion stings are defined as the injury caused by the venomous sting of a scorpion. The venom contains a variety of compounds, including peptides, proteins, and enzymes, which can cause necrosis, inflammation, and pain. Scorpion stings can affect various parts of the body, including the skin, muscles, and organs.
Causes of Scorpion Stings:
Scorpion stings are caused by the venomous spines on the scorpion's tail. When the scorpion stings, it uses its tail to pierce the skin and inject the venom into the body. The venom can cause a range of symptoms, depending on the type of scorpion and the severity of the sting. Some common causes of scorpion stings include:
1. Scorpion bites: When a scorpion bites, it injects its venom into the body through its fangs.
2. Accidental contact: Scorpions may sting when they are disturbed or threatened, such as when someone accidentally steps on them or touches them.
3. Medical procedures: In some cases, scorpion stings may be intentionally administered as part of medical procedures, such as in the treatment of certain respiratory conditions.
Symptoms of Scorpion Stings:
The symptoms of scorpion stings can vary depending on the type of scorpion and the severity of the sting. Some common symptoms include:
1. Pain: Scorpion stings can cause severe pain, which may be felt locally at the site of the sting or more generally throughout the body.
2. Swelling: The area around the sting may become swollen and inflamed.
3. Redness: The skin around the sting may turn red and warm to the touch.
4. Itching: Some people may experience itching or a burning sensation at the site of the sting.
5. Blisters: Scorpion venom can cause blisters to form on the skin.
6. Numbness: In some cases, scorpion venom may cause numbness or tingling sensations in the face, arms, or legs.
7. Breathing difficulties: Scorpion venom can cause breathing difficulties, especially in children and people with pre-existing respiratory conditions.
8. Cardiac problems: In severe cases, scorpion venom can cause cardiac problems, such as abnormal heart rhythms or even heart failure.
9. Neurological symptoms: Some scorpion venoms can cause neurological symptoms, such as headaches, dizziness, and confusion.
10. Seizures: In rare cases, scorpion stings may cause seizures.
Treatment of Scorpion Sting
---------------------------
If you suspect that you or someone else has been stung by a scorpion, seek medical attention immediately. Here are some general treatment guidelines:
1. Remain calm: Try to remain as calm as possible and do not panic.
2. Remove the stinger: Gently remove the stinger from the skin using tweezers or a credit card. Avoid squeezing the stinger, as this can release more venom.
3. Clean the wound: Wash the wound with soap and water to prevent infection.
4. Apply ice: Apply an ice pack or cold compress to reduce swelling and pain.
5. Elevate the affected area: Elevate the limb or area where the sting occurred to reduce swelling.
6. Take antihistamines: Antihistamines, such as Benadryl, can help reduce itching and inflammation.
7. Use pain relief medication: Over-the-counter pain relief medication, such as acetaminophen or ibuprofen, can help relieve pain and discomfort.
8. Monitor for signs of infection: Monitor the wound for signs of infection, such as redness, swelling, increased pain, or pus. If you notice any of these symptoms, seek medical attention immediately.
9. Seek medical attention: If you experience any of the following symptoms, seek medical attention immediately:
* Difficulty breathing
* Rapid heartbeat
* Nausea and vomiting
* Abdominal pain
* Fever
* Confusion or disorientation
It is important to note that some scorpion stings can cause severe reactions, and in rare cases, can be fatal. If you suspect that you or someone else has been stung by a dangerous scorpion, do not hesitate to seek medical attention immediately.
Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.
The symptoms of coronary disease can vary depending on the severity of the condition, but may include:
* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back
Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.
Preventative measures for coronary disease include:
* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.
* Pain during bowel movements
* Bleeding during bowel movements
* Itching or burning sensation around the anus
* Discharge of pus from the anus
* Redness and swelling around the anus
Fissure in ano can be caused by straining during bowel movements, constipation, diarrhea, or any other condition that puts pressure on the anal skin. Treatment for fissure in ano includes:
* Increasing fiber intake to soften stools and reduce constipation
* Drinking plenty of water to keep the stools soft
* Avoiding straining during bowel movements
* Using stool softeners or laxatives if necessary
* Applying a topical cream or ointment to reduce pain and promote healing
* In some cases, prescription medications may be used to treat fissure in ano.
It is important to seek medical attention if you experience any symptoms of fissure in ano, as it can lead to complications such as infection or narrowing of the anus if left untreated. A healthcare professional can diagnose fissure in ano by examining the anus and performing a physical rectal examination.
In addition to medical treatment, there are some self-care measures that can help manage symptoms of fissure in ano, such as:
* Soaking in a warm bath for 10-15 minutes several times a day to reduce pain and promote healing
* Applying a cold compress or ice pack to the affected area to reduce pain and swelling
* Avoiding spicy or irritating foods and drinks
* Using stool softeners or laxatives as directed by a healthcare professional.
It is important to note that fissure in ano can be a recurring condition, so it is important to take steps to prevent recurrence, such as maintaining a high fiber diet and drinking plenty of fluids.
Nitroglycerin
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Coronary ischemia
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Gyttorp
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James Edward Cottrell
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Johann Konrad Dippel
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Phenylketonuria
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Torpedo (petroleum)
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Jonathan Stamler
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National Institutes of Health Clinical Center
Diagnostic and prognostic role of nitroglycerin-induced dilation in patients with suspected vasospastic angina, combined with...
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How should patients take their nitroglycerin sublingual tablet?
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Doses of nitroglycerin2
Tablets8
- Your health care provider may have prescribed nitroglycerin tablets or spray for severe attacks. (nih.gov)
- Canada is experiencing a shortage of nitroglycerin tablets due to an increase in demand caused by the nitroglycerin spray shortage. (canada.ca)
- Nitroglycerin tablets are placed under the tongue and are used to treat pain during episodes of angina (chest pain) in people who have coronary artery disease (narrowing of the blood vessels that supply blood to the heart). (canada.ca)
- Nitroglycerin is rapidly absorbed following sublingual administration of nitroglycerin sublingual tablets. (nih.gov)
- The absolute bioavailability of nitroglycerin from nitroglycerin sublingual tablets is approximately 40% but tends to be variable due to factors influencing drug absorption, such as sublingual hydration and mucosal metabolism. (nih.gov)
- 2. Nitroglycerin can be given in many routes 👍 It is available in sublingual tablets , sprays, ointments, injections, and patches. (combatmedicine101.com)
- Nitrostat (nitroglycerin) 2.5mg tablets price is the best on our website. (completeonlinepharmacy.com)
- 15059. Adulteration and misbranding of tincture cinchona, fluidextract colchicuin seed, tincture belladonna leaves, morphine sulphate tablets, and nitroglycerin tablets. (nih.gov)
Subjects receiving nit1
- In one well-controlled clinical trial, subjects receiving nitroglycerin appeared to exhibit a rebound or withdrawal effect, so that their exercise tolerance at the end of the daily drug-free interval was less than that exhibited by the parallel group receiving placebo. (nih.gov)
Sublingual tablet6
- Nitroglycerin sublingual tablet is available as both a generic and a brand-name drug. (healthline.com)
- Nitroglycerin sublingual tablet is used to stop or prevent angina (chest pain). (healthline.com)
- Nitroglycerin sublingual tablet is a prescription drug that's available as the brand-name drug Nitrostat. (healthline.com)
- Nitroglycerin sublingual tablet can interact with other medications, vitamins, or herbs you may be taking. (healthline.com)
- Although nitroglycerin has historically been administered as a sublingual tablet and/or spray, it is often given intravenously in the emergency department as this enables titration to effect with predictable pharmacokinetics . (bvsalud.org)
- How should patients take their nitroglycerin sublingual tablet? (ptceprep.com)
Plasma nitroglycerin2
- Reliable assay techniques for plasma nitroglycerin levels have only recently become available, and studies using these techniques to define the pharmacokinetics of oral nitroglycerin preparations have not been reported. (nih.gov)
- Maximum plasma nitroglycerin concentrations (C max ) and area under the plasma concentration-time curves (AUC) increase dose-proportionally following 0.3 to 0.6 mg nitroglycerin. (nih.gov)
Relaxation of vascular smooth2
Generic3
- Generic nitroglycerin is used to treat angina in people with coronary artery disease. (completeonlinepharmacy.com)
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Chest pain3
- Nitroglycerin is used to treat angina (chest pain). (healthline.com)
- Nitroglycerin , a fast-acting vasodilator , is commonly used as a first-line agent for angina in the emergency department and to manage chest pain due to acute coronary syndromes . (bvsalud.org)
- Nitroglycerin also treats chest pain. (nih.gov)
Nitrate3
- The first products in the metabolism of nitroglycerin are inorganic nitrate, and the 1,2- and 1,3-dinitroglycerols. (nih.gov)
- Presumably, the studied 1-week and 2-week regimens of oral nitroglycerin therapy achieved adequate nitrate-free intervals by non-uniformity of dosing interval, with longer intervals overnight. (nih.gov)
- Nitroglycerin, an organic nitrate, is a vasodilating agent. (nih.gov)
Coronary1
- Nitroglycerin, or nitrates, can make it easier for your heart to pump blood and to improve blood flow through your coronary arteries. (nih.gov)
Isosorbide1
- The long acting nitrates isosorbide dinitrate and isosorbide 5-mononitrate now share all the beneficial effects of nitroglycerin in patients with stable and unstable angina and in selected patients with heart failure. (nih.gov)
Dilation1
- Although venous effects predominate, nitroglycerin produces, in a dose-related manner, dilation of both arterial and venous beds. (nih.gov)
Active ingredient2
- 1. It was used as an explosive first 💣Invented in 1847, nitroglycerin has been used as an active ingredient in the manufacture of explosives , mostly dynamite , and as such it is employed in the construction , demolition , and mining industries. (combatmedicine101.com)
- Friendly support ️ ️ sildenafil citrate sildenafil use street drugs, secure and nitroglycerin instead of the active ingredient in order viagra tested for here. (kidspressmagazine.com)
Mechanism of Act1
- In this review article, we outline the indications, mechanism of action, contraindications , and adverse effects of nitroglycerin as well as review relevant literature and make general recommendations regarding the use of nitroglycerin in the emergency department . (bvsalud.org)
Nitric oxide2
- Nitroglycerin forms free radical nitric oxide (NO) which activates guanylate cyclase, resulting in an increase of guanosine 3'5' monophosphate (cyclic GMP) in smooth muscle and other tissues. (nih.gov)
- Nitroglycerin is converted to nitric oxide , a potent vasodilator , in the body, leading to venodilation at lower dosages and arteriodilation at higher dosages that results in both preload and afterload reduction, respectively. (bvsalud.org)
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Nitrates1
- Nitroglycerin belongs to a class of drugs known as nitrates. (kaiserpermanente.org)
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Angina pectoris1
- Nitroglycerin (Glyceroltrinitrate) was synthetized by Ascanio Sobrero 1846 and was studied by Brunton, Tate, and Murrel who published his paper on the treatment of angina pectoris in 1879. (nih.gov)
Tolerance2
- As noted above, careful studies with other formulations of nitroglycerin have shown that maintenance of continuous 24-hour plasma levels of nitroglycerin results in insurmountable tolerance. (nih.gov)
- however, humans develop a tolerance to and dependence on nitroglycerin after long-term exposure. (combatmedicine101.com)
Vasodilator1
- Nitroglycerin acts as a vasodilator. (guidetopharmacology.org)
Patients2
- Sir William Osler was the first who suggested the use of nitroglycerin in patients with congestive heart failure "when the pulse is hard and firm", in his "Principles and Practice of Medicine" 1892. (nih.gov)
- Patients have received either dexmedetomidine , magnesium sulfate or nitroglycerine. (bvsalud.org)
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Drugs4
- Nitroglycerin belongs to a class of drugs called vasodilators. (healthline.com)
- Examples of drugs that can cause interactions with nitroglycerin are listed below. (healthline.com)
- Taking any of these drugs with nitroglycerin can cause very low blood pressure. (healthline.com)
- Very low blood pressure may result from taking nitroglycerin with other medicines whose action also lowers blood pressure, such as drugs used to treat erectile dysfunction. (medlineplus.gov)
Tongue1
- may get heparin (or another blood thinner) and nitroglycerin (under the tongue or through an IV). (nih.gov)
Pulmonary1
- Elevated central venous and pulmonary capillary wedge pressures, and pulmonary and systemic vascular resistance are also reduced by nitroglycerin therapy. (nih.gov)
Heart2
- Nitroglycerin is a medicine that helps relax the blood vessels leading to the heart. (medlineplus.gov)
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Magnesium4
- The aim of the current study was to compare magnesium sulphate and dexmedetomidine with nitroglycerin as regard hypotensive effect as primary outcome, volume of blood loss, blood substitution and pattern of recovery as secondary outcome during lumbar spine surgery . (bvsalud.org)
- 0.000) with duration of surgery between different study groups with duration of surgery shortest in dexmedetomidine group followed by magnesium sulfate group and then nitroglycerine group. (bvsalud.org)
- There were highly significant differences between different study groups with fluid maintenance with higher volume in nitroglycerine group then magnesium sulfate group and then dexmedetomidine group. (bvsalud.org)
- 0.000) with systolic blood pressure between study groups at A1 and hypotensive agent discontinuation with lowest systolic blood pressure in dexmedetomidine group followed by magnesium sulfate group and then nitroglycerine group. (bvsalud.org)
Medicines1
- Medicines with other names may also contain nitroglycerin. (medlineplus.gov)
Drug1
- An overnight hospital stay may be needed if a long-acting nitroglycerine drug preparation caused the overdose. (medlineplus.gov)
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Explosive1
- Nitroglycerin - This article is about the chemical properties of nitroglycerin and its use as an explosive. (en-academic.com)
Dizziness1
- Nitroglycerin can cause dizziness during the first few hours after you take it. (healthline.com)
Occur1
- Mean peak nitroglycerin plasma concentrations occur at a mean time of approximately 6 to 7 minutes postdose (Table 1). (nih.gov)
Symptoms1
- Below are symptoms of a nitroglycerin overdose in different parts of the body. (medlineplus.gov)
Rapid1
- The volume of distribution of nitroglycerin is about 3 L/kg, and nitroglycerin is cleared from this volume at extremely rapid rates, with a resulting serum half-life of about 3 minutes. (nih.gov)
Medicine1
- Nitroglycerin overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
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Medications1
- Nitroglycerin is in a class of medications called vasodilators. (nih.gov)
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Medical1
- with rest or within 3 minutes of taking nitroglycerin , call for emergency medical help. (nih.gov)