Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antianginal drugs were evaluated on the basis of their ability to protect against subepicardial electrogram changes induced by local ventricular ischemia in anesthetized dogs. Sch 11973 [N-(2-phenylisopropyl)-N-p-toluene sulfonyl urea], a potential new antianginal agent, was also effective against local ventricular ischemia with its maximum effect appearing at 1mg/kg, i.v. or i.d. and with a duration of at least 2 hours. Nitroglycerin, at a dose of 0.04 mg/kg given bucally, exerted less protection, lasting on the average less than 15 minutes. Protection by propranolol at 1 mg/kg, i.v., was not better than nitroglycerin, but lasted up to one hour, while dipyridamole was ineffective when given in a dose range of 0.1-10 mg/kg, i.v. Sch 11973 differed from standard antianginal agents which may act via beta-adrenergic blocking activity or alteration of cardiac or circulatory dynamics since no acute pharmacological changes were observed after Sch 11973 was administered.
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PMID:Pharmacology of Sch 11973, N-(2-phenylisopropyl)-N-p-toluene sulfonyl urea, a potential new antianginal agent. 2 76

Chronically instrumented awake dogs were used to study the effects of nitroglycerin and propranolol on the transmural distribution of myocardial blood flow during transient ischemia. Studies were carried out 7-14 d after implantation of an electromagnetic flowmeter probe and balloon occluder on the left circumflex coronary artery, placement of epicardial minor axis sonar crystals, and implantation of left atrial, left ventricular, and aortic catheters. The occluder was inflated to completely interrupt flow for 10 s followed by partial release to reestablish flow at 60% of the preocclusion level. During this partial release, which served as the control for the study, regional myocardial blood flow was measured with 7- to 10-mum radioactive microspheres. After control measurements, seven dogs were given nitroglycerin (0.4 mg i.v.) and eight dogs propranolol (0.2 mg/kg i.v.). 5 min later the occlusion and partial release sequence was repeated, and regional myocardial blood flow was measured when heart rate, aortic and left ventricular end-diastolic pressure, and minor axis diameter were unchanged from control values.The data values were selected so that total flow to the ischemic region during partial release after nitroglycerin or propranolol administration was not significantly different from flow during the control partial release. After nitroglycerin administration, endocardial flow (endo) in the ischemic region increased from 0.46+/-0.07 to 0.59+/-0.06 ml/min per g (P < 0.006); epicardial flow (epi) decreased from 0.78+/-0.09 to 0.70+/-0.08 ml/min per g (P < 0.04). The endo:epi ratio increased from 0.65+/-0.07 to 0.92+/-0.10 (P < 0.05). In contrast, administration of propranolol produced no significant change in transmural flow (endo, 0.42+/-0.02 and 0.46+/-0.03 ml/min per g; epi, 0.71+/-0.06 and 0.70+/-0.07 ml/min per g) or in the endo:epi ratio (0.60+/-0.03, 0.66+/-0.06) in the ischemic region. Nitroglycerin and propranolol produce different effects on the transmural distribution of blood flow to ischemic myocardium. Nitroglycerin can increase blood flow to the underperfused endocardium in the absence of alterations in heart size, hemodynamic parameters, and total transmural flow to the ischemic region. Under similar conditions, propranolol has no significant effect on the transmural distribution of blood flow to an ischemic region.
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PMID:Effects of nitroglycerin and propranolol on the distribution of transmural myocardial blood flow during ischemia in the absence of hemodynamic changes in the unanesthetized dog. 10 67

The significance of asymptomatic episodes of ischemic type S-T segment depression was studied in 20 patients with coronary heart disease. Continuous 10 hour electrocardiographic recordings accompanied by detailed daily diaries of activity and symptoms were obtained periodically during a mean time of 16 months. All patients had ischemic type S-T depression associated with angina pectoris during treadmill exercise. Measurements of heart rate, S-T depression and exercise level at the onset of angina obtained during repeated controlled exercise tests at the start of each study period were compared with the measurements recorded during daily activity. After 2,826 hours of recording, 411 transient epidsodes of ischemic type S-T depression were noted during usual daily activity. Only 101 (25 percent) of these episodes were associated with angina. The remaining episodes were unrelated to other symptoms or to posture. All occurred at heart rates significantly lower than those observed at the onset of angina during exercise testing. Of these episodes of asymptomatic S-T depression, 72 percent occurred only at rest or during very light activity such as slow walking or sitting. Nitroglycerin administered hourly significantly reduced the frequency of these episodes, thus supporting the concept that they represent painless ischemia. Because the episodes of asymptomatic ischemic type S-T depression occurred more frequently than angina during usual daily activity and were evident at heart rates and activity levels well below those expected to evoke ischemia, they may be caused by factors other than those that cause angina.
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PMID:Transient asymptomatic S-T segment depression during daily activity. 40 3

The systemic hemodynamic and myocardial effects of potent vasodilators administered directly into the left coronary artery were determined and compared with the actions of contrast material in 10 anesthetized dogs in the normal state and in the presence of segmental myocardial ischemia. Contrast material (Renografin 76) caused systemic hypotension, rise in left ventricular diastolic pressure and decreases in LV dp/dt and dp/dt/LVP in both states. Doses of ATP (7.2 microgram/kg and 20 microgram/kg/min) which are maximally effective in augmenting coronary blood flow caused only mild arterial hypotension and minimal inotropic effects in both states. Nitroglycerin (3 microgram/kg and 10 microgram/kg/min) induced no inotropic effects but slightly greater arterial hypotension than ATP in both states. On the other hand, papaverine HCl (300 microgram/kg and 800 microgram/kg/min) induced profound increases in LV dp/dt and dp/dt/LVP, decreases in LVEDP and arterial hypotension in the non-ischemic state. In the presence of segmental ischemia, papaverine HCl caused significantly less increases in LV dp/dt and dp/dt/LVP, paradoxical increases in LVEDP in 5 dogs and ventricular fibrillation in 3 dogs. Thus, maximally effective vasodilatory doses of ATP causes only small alterations in hemodynamics and myocardial contractile state of the normal and ischemic heart. Similar doses of papaverine induce profound positive inotropic effects which are apparently deleterious to the ischemic heart.
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PMID:Comparative hemodynamic effects of coronary vasodilators and contrast material on the normal and ischemic canine myocardium: determination of the optimal agent for clinical augmentation of coronary blood flow. 40 73

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.
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PMID:Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease. 80 82

Nitroglycerin reduces ischemic injury during acute myocardial infarction (AMI) in dogs--an effect that is potentiated when drug-induced hypotension and tachycardia are prevented with phenylephrine. To determine the effectiveness of nitroglycerin, alone or with phenylephrine, during AMI in man, 12 patients (five or whom had left heart failure) were evaluated by summing ST-segment abnormalities (sigmaST) from 35 precordial electrodes. The seven patients without heart failure did not benefit consistently from nitroglycerin alone; however, addition of phenylephrine to abolish nitroglycerin-induced arterial pressure reduction uniformly diminished sigmaST (4.9 to 3.2 mv; P less than 0.05). In patients with heart failure, nitroglycerin alone consistently reduced ischemia (5.8 to 4.4 mv, P less than 0.05); addition of phenylephrine often partially reversed this effect. Thus, administration of nitroglycerin, alone or with phenylephrine, can reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends on the presence or absence of left ventricular failure before treatment.
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PMID:Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction. 80 12

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 nitroglycerin on left ventricular hemodynamics were determined in ten patients from biplane cineventriculograms and simultaneous pressure measurements. Before and after nitroglycerin (1.6 mg sublingually) the following parameters were measured: Systolic (PLV) and enddiastolic pressure (PLVED), enddiastolic (EDV) und endsystolic volume (ESV), cardiac output (SV), ejection fraction (EF) and ejection rate (ER), ejection time (tej), heart rate (HR), dp/dtmax, dp/dtmax Pi-Ped, maximal systolic wall stress (sigmamax), integrated systolic wall stress (sigma), outflow resistance (Rsys) and ventricular compliance (a). Nitroglycerin leads to a reduction of both, pre- and afterload, with a significant fall of PLV (10.8%), PLVED (21.8%), EDV (9.1%) ESV (13.3%) AND Rsys (14.4%). The changes of ventricular pressure and geometry result in a diminution of left ventricular wall stress (sigmamax- 11.8%, sigma - 26.4%), representing a decrease of calculated total oxygen-consumption of 11.5%. In six patients with reduced left ventricular diastolic compliance nitroglycerin leads to a remarkable increase of the compliance. This is probably due to the reversal of a latent ischemia by the decreased myocardial oxygen-consumption.
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PMID:[Influence of nitroglycerin on hemodynamics, wall tension and oxygen consumption of the left ventricle]. 82 24

Nitroglycerin has dependable, short-lived veno- and arterial vasodilatory effects ameliorating ischemia through both preload reduction and coronary vasodilation. Nitroglycerin should be used prior to left ventriculography in patients with elevated left ventricular end-diastolic pressure. The arterial pressure waveform alteration of nitroglycerin can be explained on the basis of changes in arterial distensibility and reflected wave patterns and may vary considerably among individuals with different degrees of atherosclerosis.
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PMID:Interpretation of cardiac pathophysiology from pressure waveform analysis: effects of nitroglycerin. 157 82

To evaluate the degree to which nitroglycerin reduces myocardial ischemia and dysfunction induced by transient coronary occlusion, 19 patients were studied during coronary angioplasty of the left anterior descending coronary artery. After a control occlusion of 60 seconds, 0.2 mg nitroglycerin was administered intravenously and the occlusion was repeated for 60 seconds. Before and during the occlusion period, pulmonary capillary wedge pressure was measured, the intracoronary ECG was recorded, and ventricular volumes, ejection fraction, and regional systolic shortening were obtained by digital subtraction angiography. Nitroglycerin caused a significant fall in pulmonary capillary wedge pressure before (10 vs. 7 mmHg) and at 60 seconds occlusion (18 vs. 14 mmHg), but did not significantly delay the rise in wedge pressure (37 vs. 44 seconds). End-systolic left ventricular volume at 60 seconds of occlusion was reduced by nitroglycerin (77 vs. 68 ml), whereas regional shortening of the ischemic segments remained unchanged (22 vs. 23%). Nitroglycerin did not delay the onset of ischemic ST-segment elevation (14 vs. 14 seconds) and had no effect on the changes of ST elevation in the intracoronary ECG (1.9 vs. 1.9 mV). These findings suggest that intravenous nitroglycerin reduces filling pressure and slightly improves left ventricular global function during acute coronary occlusion. Nitroglycerin, however, has little effect on ischemia-induced regional dysfunction and on ST-segment elevation in the intracoronary ECG.
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PMID:The effects of pretreatment with nitroglycerin on ischemic left ventricular dysfunction during coronary angioplasty. 190 35


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