Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from DRUG RESISTANCE wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from MAXIMUM TOLERATED DOSE and NO-OBSERVED-ADVERSE-EFFECT LEVEL.Administration, Cutaneous: The application of suitable drug dosage forms to the skin for either local or systemic effects.Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Administration, Sublingual: Administration of a soluble dosage form by placement under the tongue.Nicorandil: A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.Coronary Vessels: The veins and arteries of the HEART.Pentaerythritol Tetranitrate: A vasodilator with general properties similar to NITROGLYCERIN but with a more prolonged duration of action. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1025)Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)Aldehyde Dehydrogenase: An enzyme that oxidizes an aldehyde in the presence of NAD+ and water to an acid and NADH. This enzyme was formerly classified as EC 1.1.1.70.Tilt-Table Test: A standard and widely accepted diagnostic test used to identify patients who have a vasodepressive and/or cardioinhibitory response as a cause of syncope. (From Braunwald, Heart Disease, 7th ed)Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Angina Pectoris: The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.Peripheral Nervous System Agents: Drugs that act principally at one or more sites within the peripheral neuroeffector systems, the autonomic system, and motor nerve-skeletal system. (From Smith and Reynard, Textbook of Pharmacology, 1991, p75)Coronary Circulation: The circulation of blood through the CORONARY VESSELS of the HEART.Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons.Ferricyanides: Inorganic salts of the hypothetical acid, H3Fe(CN)6.Vascular Resistance: The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries.Coronary Vasospasm: Spasm of the large- or medium-sized coronary arteries.Acetylcholine: A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Nitric Oxide Donors: A diverse group of agents, with unique chemical structures and biochemical requirements, which generate NITRIC OXIDE. These compounds have been used in the treatment of cardiovascular diseases and the management of acute myocardial infarction, acute and chronic congestive heart failure, and surgical control of blood pressure. (Adv Pharmacol 1995;34:361-81)Isosorbide Dinitrate: A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.Nitrates: Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.Cyclic GMP: Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)Syncope, Vasovagal: Loss of consciousness due to a reduction in blood pressure that is associated with an increase in vagal tone and peripheral vasodilation.Nitroprusside: A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.Muscle Relaxation: That phase of a muscle twitch during which a muscle returns to a resting position.Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2.Methylene Blue: A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits GUANYLATE CYCLASE, and has been used to treat cyanide poisoning and to lower levels of METHEMOGLOBIN.Injections, Intra-Arterial: Delivery of drugs into an artery.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.Infusions, Intravenous: The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.Double-Blind Method: A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.Scorpion Stings: The effects, both local and systemic, caused by the bite of SCORPIONS.Coronary Disease: An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.Fissure in Ano: A painful linear ulcer at the margin of the anus. It appears as a crack or slit in the mucous membrane of the anus and is very painful and difficult to heal. (Dorland, 27th ed & Stedman, 25th ed)Cyanamide: A cyanide compound which has been used as a fertilizer, defoliant and in many manufacturing processes. It often occurs as the calcium salt, sometimes also referred to as cyanamide. The citrated calcium salt is used in the treatment of alcoholism.Radial Artery: The direct continuation of the brachial trunk, originating at the bifurcation of the brachial artery opposite the neck of the radius. Its branches may be divided into three groups corresponding to the three regions in which the vessel is situated, the forearm, wrist, and hand.Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.Blood Flow Velocity: A value equal to the total volume flow divided by the cross-sectional area of the vascular bed.Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium.Vasoconstriction: The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.S-Nitrosothiols: A group of organic sulfur-containing nitrites, alkyl thionitrites. S-Nitrosothiols include compounds such as S-NITROSO-N-ACETYLPENICILLAMINE and S-NITROSOGLUTATHIONE.Aorta: The main trunk of the systemic arteries.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.

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)

  • Patients with obstructive hypertrophic cardiomyopathy, pronounced hypovolemia, STEMI or presumed cardiac chest pain, inferior myocardial infarction with right ventricular involvement, raised intracranial pressure, cardiac tamponade, and patients taking certain drugs for erectile dysfunction (phosphodiesterase inhibitors), pregnancy, or with a known allergy to nitroglycerin will be excluded from the study. (clinicaltrials.gov)
  • Nitroglycerin is a vasodilator, a medicine that opens blood vessels to improve blood flow. (uncmedicalcenter.org)
  • Nitroglycerin is a drug indicated for use with cardiogenic pulmonary edema, as it is a quick and potent vasodilator, which leads to preload and afterload reduction. (picmonic.com)
  • Nitroglycerin is also used medically as a vasodilator to treat heart conditions, such as angina and chronic heart failure . (curecrowd.com)
  • The research team led by Jonathan Stamler, M.D., HHMI investigator at Duke, found an enzyme that not only breaks down nitroglycerin and releases a nitric oxide-related molecule, but whose action is suppressed in blood vessels made tolerant after repeated doses of nitroglycerin. (emaxhealth.com)
  • 2. Methods: A convenience sample of patients presenting to the Emergency Department will be randomized to receive either sublingual 0.4 mg doses of nitroglycerin or placebo. (clinicaltrials.gov)
  • Whenever these abscesses are diagnosed, nitroglycerin ointment buy online systemic antimicrobial therapy should be administered in large doses. (kidselitesports.org)
  • Keep an eye on eminence and trough serum levels 48 hours after start remedial programme and every 3-4 days thereafter as properly as after chang- ing doses order genuine nitroglycerin on-line. (bmfa.org)
  • Nitroglycerin also causes arteriolodilation at higher doses. (picmonic.com)
  • Nitroglycerin would be problematic, as it appears that this patient might be having a right ventricular infarct, and lowering right-sided filling pressures with nitroglycerin may lead to severe hypotension. (thefreedictionary.com)
  • Sit or lie down to take your nitroglycerin. (uncmedicalcenter.org)
  • You can also take your nitroglycerin once to help prevent angina before you start doing activities that you know will bring on your angina. (ucsd.edu)
  • Sit down before you take your nitroglycerin. (ucsd.edu)
  • These workers then develop a tolerance to nitroglycerin after exposure through the week and feel fine. (picmonic.com)
  • According to a double-blind study of 48 individuals, use of vitamin C at a dose of 2000 mg three times daily helped maintain the effectiveness of nitroglycerin. (portsmouthhospital.com)
  • Simulated plasma concentration-time profiles were reasonably fitted to the observed concentrations of nitroglycerin and its two metabolites after transdermal administration. (elsevier.com)
  • The pharmacokinetics and pharmacodynamics of nitroglycerin and aspirin have been evaluated with emphasis being placed on the in vitro and in vivo metabolism of these drugs in various tissues of the body. (edu.au)
  • Now, not only have researchers from Howard Hughes Medical Institute (HHMI) and Duke University Medical Center solved this age-old riddle, they have also shed light on the second major mystery surrounding nitroglycerin, why patients eventually develop a tolerance to the drug's effects. (emaxhealth.com)
  • Additionally, there is no data from clinical trials showing that nitroglycerin actually improves outcomes for heart patients, and there is reason to believe that nitroglycerin may even adversely affect these patients," Stamler said. (emaxhealth.com)
  • Nitroglycerin has an excellent safety profile if used in patients with adequate pretreatment blood pressures. (clinicaltrials.gov)
  • Henrikson and colleagues (1) concluded that pain relief by nitroglycerin did not predict disease in 459 patients admitted to the hospital for work-up of possible ischemic heart disease. (annals.org)
  • Nitroglycerin was given intravenously to 5 anesthetized, hyperventilated (PaCO 2 25 to 30 torr) patients during craniotomy, to facilitate surgery by creating a relatively bloodless field, and to decrease the potential need for blood transfusion. (elsevier.com)
  • Nitroglycerin can lead to tachycardia in many patients. (picmonic.com)
  • If you are giving tPA to patients with STEMI, it is wise to avoid IV nitroglycerine. (blogspot.com)
  • Concurrent nitroglycerine therapy impairs tissue-type plasminogen activator-induced thrombolysis in patients with acute myocardial infarction. (blogspot.com)
  • The present study was conducted to determine whether such an interaction between nitroglycerin and t-PA occurs in patients with acute myocardial infarction undergoing thrombolytic treatment. (blogspot.com)
  • These observations indicate that nitroglycerin given with t-PA significantly decreases the plasma t-PA antigen concentrations and impairs the thrombolytic effect of t-PA in patients with acute myocardial infarction. (blogspot.com)
  • 0.05) compared with values in 7 patients receiving only nitroglycerin (Group II) and in patients receiving nitroglycerin before phenylephrine in Group I and with the values in 7 patients who received no phenylephrine. (elsevier.com)
  • From these findings, with greater nitroglycerininduced decreases in mean arterial pressure and coronary flow in patients with acute ischemia, it appears that phenylephrine with nitroglycerin may particularly improve myocardial energetics. (elsevier.com)
  • To evaluate efficacy of intravenous nitroglycerine to attenuate hemodynamics to laryngoscopy and endotracheal intubation in healthy, normotensive ASA grade I patients. (innovativepublication.com)
  • To improve blood flow to the heart, nitroglycerin opens up (dilates) the arteries in the heart ( coronary arteries ), which improves symptoms and reduces how hard the heart has to work. (uncmedicalcenter.org)
  • In each subject, the emptying of 300 ml of 25% glucose labeled with 99mTc was assessed on two separate days during intravenous infusion of either nitroglycerin (5 micrograms/min in 5% dextrose) or 5% dextrose (control). (edu.au)
  • While it is known that nitric oxide, a breakdown product of nitroglycerin, plays a critical role regulating blood vessel relaxation, scientists still did not know the mechanism by which nitric oxide is generated from the nitroglycerin molecule, which in fact shows little resemblance to nitric oxide. (emaxhealth.com)
  • Moreover, by understanding the molecular mechanism of nitroglycerin bioactivation and tolerance, it may now be possible to design and develop novel nitrovasodilator drugs that do not cause tolerance. (emaxhealth.com)
  • Nitroglycerin is contraindicated for use in combination with Viagra (sildenafil). (picmonic.com)