Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitroglycerin (0.5 mg) was administered sublingually either before (n = 10) or after (n = 10) a standard contraction meal (200 ml of cream) during oral cholecystography. In both groups the standard contraction meal caused a significant contraction of the gallbladder. Nitroglycerin had no significant dilatation effect; hence its benefit during an acute attack of pain in a patient with gallstones seems to be questionable.
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PMID:The effect of sublingually administered nitroglycerin on the contraction of the human gallbladder. 10 Apr 29

1. A quantitative in vitro study has been made of the actions of glyceryl trinitrate and sodium nitrite on vascular smooth muscle (dog femoral artery and saphenous vein; rat portal vein); these have been compared with the actions of papaverine, isoprenaline, salbutamol, pentaerythritol tetranitrate and trimetazidine. 2. Glyceryl trinitrate was more active on the saphenous vein than on the femoral artery in inhibiting noradrenaline and potassium-induced tone. 3. Unlike glyceryl trinitrate, sodium nitrite and isoprenaline, papaverine and diazoxide inhibited noradrenaline-induced contractions of venous and arterial smooth muscle to the same extent. 4. The selective dilator effects of glyceryl trinitrate on venous smooth muscle may explain its action in alleviating the pain of angina pectoris. It is suggested that the use of these three vascular smooth muscle preparations (arterial, and veins with and without spontaneous myogenic activity) is a useful initial screening procedure for prospective antianginal drugs acting by venodilatation.
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PMID:Comparative effects of glyceryl trinitrate on venous and arterial smooth muscle in vitro; relevance to antianginal activity. 40 60

Of 88 consecutive patients aged 20 to 77 years with severe symptomatic aortic valve disease requiring surgery, 51 patients had angina pectoris; of these 51, 41 had predominant aortic stenosis and 10 had severe aortic regurgitation. All patients with angina pectoris underwent coronary angiography; significant coronary arterial disease was encounted in 24 per cent of those with aortic stenosis and 20 per cent of those with aortic regurgitation. By contrast, of 37 patients without angina pectoris 19 underwent coronary arteriography; none showed significant coronary artery disease (P smaller than 0.05). Among patients with angina pectoris, 17 per cent of those with aortic stenosis experienced prolonged, rest or nocturnal pain, compared to 70 per cent of those with aortic regurgitation (P smaller than 0.005). At the time of onset of angina pectoris, there were features of heart failure in 34 per cent of those with aortic stenosis, and in 90 per cent of those with aortic regurgitation (P smaller than 0.005). Nitroglycerin promptly relieved angina pectoris in 56 percent of patients with aortic stenosis and in 50 per cent of those with aortic regurgitation (P smaller than 0.05). Neither the pattern of angina pectoris nor the response to nitroglycerin was dependent upon the coexistence of significant coronary artery disease. In patients with aortic stenosis, there was not significant difference between those with angina pectoris, and those without angina with regard to left ventricular end-diastolic volume, end-diastolic pressure, ejection fraction, peak systolic pressure, wall thickness, cardiac index, or the product of these factors. In patients with aortic regurgitation, cardiac index was significantly lower (P smaller than 0.05), left ventricular end-diastolic volume tended to be larger, and ejection fraction tended to be lower in patients with angina pectoris as opposed to those without angina pectoris.
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PMID:Clinical, haemodynamic, and coronary angiographic correlates of angina pectoris in patients with severe aortic valve disease. 80 13

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.
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PMID:Protection of ischemic myocardium by nitroglycerin: experimental and clinical results. 81 59

The effects of N-acetylcysteine, a sulfhydryl group donor, on nitroglycerin-induced headache and dilation of temporal and radial arteries were investigated in 11 healthy volunteers. Nitroglycerin, 0.06 microgram/kg/min, was infused for 20 minutes immediately after and 120 minutes after pretreatment with N-acetylcysteine (100 mg/kg) or placebo. Arterial diameters were measured with high frequency ultrasound, and pain was scored by use of a previously evaluated 10-point scale. Plasma levels of free (n = 2) and total (n = 11) N-acetylcysteine were determined. N-Acetylcysteine potentiated the headache response (median headache score, 3 versus 1), and the headache retained its vascular characteristics. Temporal artery dilation was also potentiated by N-acetylcysteine, 139% +/- 3% versus 127% +/- 3% of baseline, whereas the radial artery was unaffected. The potentiation was most pronounced after the first nitroglycerin infusion (12% versus 4.5% compared with placebo). A prolonged dilation of the temporal artery was observed only after the first nitroglycerin infusion, when high levels of N-acetylcysteine were present.
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PMID:N-acetylcysteine enhances nitroglycerin-induced headache and cranial arterial responses. 150 48

Nitroglycerin (NTG) has the potential to reduce myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Buccal administration of NTG offers practical advantages compared to intravenous or intracoronary administration. In a double-blind, randomized, placebo-controlled study, 100 patients were given 5 mg of buccal NTG or placebo during PTCA. A scoring system for ischemic pain during balloon inflation was defined as pain intensity (0 to 5) multiplied by duration of pain after balloon deflation (1 = 0 to 30 seconds, 2 = 30 to 60 seconds, 3 = 60 to 120 seconds, 4 = greater than 120 seconds but subsiding, and 5 = until next inflation). Fourteen patients were excluded: 12 for vagal reaction (eight NTG and four placebo; p greater than 0.05) requiring atropine, making buccal absorption unreliable, and two for inability to dilate. Eighteen patients (nine NTG and nine placebo) had no pain during balloon inflation. Sixty-eight patients (32 NTG and 36 placebo) had ischemic pain with a pain score (mean +/- SD) of 4.8 +/- 3.8 for the NTG group versus 7.1 +/- 4.8 for the placebo group (p = 0.03). We conclude that buccal NTG significantly decreases myocardial ischemia during PTCA.
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PMID:Buccal nitroglycerin decreases ischemic pain during coronary angioplasty: a double-blind, randomized, placebo-controlled study. 169 25

A 28 yr-old male presented with chest pain and acute ST elevation following ingestion of pseudoephedrine. The pain and electrocardiographic changes disappeared after the administration of sublingual Nitroglycerin. Myocardial enzymes did show some evidence for myocardial necrosis. A subsequent coronary arteriogram showed no occlusive lesions. Pseudoephedrine, a sympathomimetic agent, may be implicated in the initiation of coronary spasm and myocardial infarction in some patients.
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PMID:Coronary artery spasm and myocardial infarction in a patient with normal coronary arteries: temporal relationship to pseudoephedrine ingestion. 234 9

The administration of nifedipine by the sublingual rather than the oral route has been suggested to provide a more rapid onset of effect. We compared the safety and efficacy of sl nifedipine to sl nitroglycerin in patients who developed anginal chest pain during diagnostic exercise stress testing. Consecutive patients undergoing diagnostic Bruce treadmill exercise who had not had a recent myocardial infarction or undergone coronary bypass graft surgery and who were not taking nitrates, beta-blockers, digoxin, or calcium antagonists were eligible. Seventy-eight patients meeting the inclusion/exclusion criteria consented to participate. Of these 78, 13 developed chest pain necessitating exercise cessation and were randomized to either nitroglycerin or nifedipine. Nitroglycerin was initially given to seven patients and nifedipine to six patients. Complete pain relief was observed in five of seven (71 percent) nitroglycerin patients at two minutes postdose. At four minutes postdose, the remaining two nitroglycerin patients were essentially pain-free. At two minutes postdose, no patient receiving nifedipine had complete pain resolution, and only one patient (17 percent) had partial (greater than 50 percent) pain relief. At four minutes postdose, four of the nifedipine patients were crossed over to nitroglycerin. At two minutes after the nitroglycerin dose, all four patients had total pain relief. The remaining two nifedipine patients had partial pain relief and were not crossed over to nitroglycerin. Subjective side effects and changes in heart rate and blood pressure were not significantly different between nitroglycerin and nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of sublingual nifedipine versus nitroglycerin in the treatment of acute angina pectoris. 250 45

The effect of high thoracic epidural anaesthesia with intermittent epidural bolus injections of bupivacaine (2.5 or 5 mg ml-1) was studied in 28 patients with unstable angina pectoris. The majority of the patients had a history of previous acute myocardial infarction(s) and/or angina pectoris and severe coronary artery disease. All patients were treated with nitroglycerin infusion for greater than 24 h and were included in the study if they had chest pain, not caused by acute myocardial infarction, at bed rest or recurrent anginal pain at rest greater than 2 days after infarction. 4.4 +/- 0.3 ml of bupivacaine induced a blockade of the upper seven sympathetic segments (Th1-7) for 98 +/- 9 min. Heart rate decreased significantly from 70 +/- 3 to 64 +/- 3 beats min-1 while blood pressure was unaffected by thoracic epidural anaesthesia. In 27 patients (96%) the anaesthesia induced complete analgesia. Nitroglycerin infusion was discontinued definitely within 3 h in 26 patients (93%) and pain was thereafter controlled by means of thoracic epidural anaesthesia as the sole treatment in 23 patients (82%) and as the major treatment in 25 patients (89%). Twenty-one patients (75%) were fully mobilized and stabilized. Treatment with thoracic epidural anaesthesia lasted for 6.0 +/- 1.1 days. The number of daily epidural injections decreased significantly with time from 2.7 +/- 0.3 the first day to 0.9 +/- 0.3 the fourth day (P less than 0.01, n = 19). Two patients developed acute myocardial infarction during the anaesthesia treatment period, and one of these patients died.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thoracic epidural anaesthesia in patients with unstable angina pectoris. 275 7

Nitroglycerin has long been a mainstay of the treatment of ischemic cardiac pain. The introduction of transdermal formulations and in particular the development of controlled methods of delivery have been responsible for the renaissance of clinical interest in this simple and effective treatment. The pathophysiologic abnormality accompanying myocardial ischemia affords a natural theater for the exhibition of the therapeutic utility of these preparations and methods. The means whereby nitrates induce relaxation of vascular smooth muscle are not entirely clear, but their pharmacodynamic activities are perfectly plain. In the doses used in clinical practice, nitrates exert their predominant hemodynamic effects and therapeutic benefits through their peripheral vasodilator activities. This is particularly marked in veins, although in higher doses nitrates also dilate the larger systemic and coronary arteries. Criticisms of the efficacy of transdermal formulations of nitrates in the treatment of angina pectoris have arisen largely from uncritical acceptance of a small number of studies of questionable methodologic validity. Large-scale general practice studies have invariably found that transdermal nitrate delivery systems improve the quality of life in ambulant patients: anginal attacks are reduced with a minimum of side effects. The widespread acceptance of this novel form of drug delivery has stimulated its application in other therapeutic avenues. The efficacy of transdermal nitroglycerin in the suppression of silent ischemic attacks has been demonstrated. The maintenance of benefit initiated by intravenous nitroglycerin in patients with unstable angina also broadens the use of this method of nitrate delivery. In patients with acute myocardial infarction, whether complicated by left ventricular failure or not, the nitrates, and transdermal nitroglycerin in particular, appear to hold considerable promise. Improvement of hemodynamic abnormalities may cause reduction in infarct size and fewer life-threatening arrhythmias. Even survival may be extended. The utility of transdermal nitrates in the treatment of severe chronic heart failure is less certain. But the use of higher doses and an interval regimen of administration may hold promise for such patients. Naturally, more information is required before the overall therapeutic profile of this new method of controlled nitroglycerin delivery across the whole spectrum of coronary heart disease can be fully described. Fortunately, the high level of efficacy and safety of transdermal nitroglycerin demonstrated in the majority of reported studies encourages the pursuit of such an important therapeutic target.
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PMID:The role of transdermal nitroglycerin in the treatment of coronary heart disease. 308 57


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