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)

In 12 patients with coronary artery disease and typical exercise-induced angina pectoris hemodynamic and ECG studies were performed at rest and during ergometer load in supine position. During the attacks of angina there was a significant ST-depression in all cases accompanied by elevated pulmonary capillary wedge pressures (PCP) and pulmonary artery mean pressures (PAM). Intravenous administration of 40 mg furosemide showed consistent hemodynamic changes. Cardiac output (CO) dropped significantly by 15.9 per cent at rest (p is less than 0.001) and by 6.9 per cent during exercise (p is less than 0.005). The PCP during exercise following furosemide decreased from 32.9 mmHg to 11.8 mm Hg (p is less than 0.001) and was paralleled by a significant decrease of PAM, indicating reduction of ischemia-related hemodynamic impairment. Furthermore, there was a striking improvement of Ecg findings during ergometer load in 9 of 12 patients as well as a relief of anginal pain in 11 of 12 patients. The present demonstration of antianginal properties of furosemide may be explained by the reduction of ventricular volumes and pressures, resulting in a decrease of myocardial wall stress. These effects are suggested to be related to the peripheral venodilator capacity of furosemide in conjunction with its diuretic properties. Thus, in patients with left ventricular dysfunction secondary to ischemia, intravenous furosemide may have salutary effects on myocardial oxygen requirements resembling the action of nitroglycerin, but without its oxygen-wasting effects on tachycardia.
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PMID:[Effects of furosemide on hemodynamic, electrocardiographic, and symptomatic responses to exercise in patients with angina pectoris (author's transl)]. 63 18

Pharmacological agents administered prior to the institution of myocardial anoxia or ischemia may protect the myocardium by preventing ATP depletion, structural damage to cell membranes and organelles, and postanoxic disturbances in coronary microcirculation. Propranolol, dipyridamole, nitroglycerin, and mannitol all have the potential to protect the myocardium in one or more of these ways and thus have promise for clinical use.
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PMID:Prevention of intraoperative myocardial injury by pretreatment with pharmacological agents. 80 68

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

This study was designed to determin the effect of nitroglycerin upon transmural distribution of myocardial blood flow in the awake dog during normal conditions and in the presence of ischemia-induced coronary vasodilation. Studies were performed in chronically prepared dogs with electromagnetic flowmeters and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow was estimated by using radionuclide-labeled microspheres, 7-10 mum in diameter, injected into the left atrium. During control conditions endocardial flow (0.86 plus or minus SEM 0.05 ml/min per g) slightly exceeded epicardial flow (0.72 plus or minus 0.03 ml/min per g, P smaller than 0.05), and this distribution of flow was not significantly altered by nitroglycerin. After a 5-s coronary artery occlusion, reactive hyperemia occurred with excess inflow of arterial blood effecting 360 plus or minus 15% repayment of the blood flow debt incurred during occlusion. When arterial inflow was limited to the preocclusion rate during coronary vasodilation after a 5-s total coronary artery occlusion, flow to the subepicardial myocardium was increased at the expense of underperfusion of the subendocardial myocardium, and the delayed reactive hyperemia was markedly augmented (mean blood flow debt repayment =775plus or minus 105%, P smaller than 0.01). Tese data suggested that subendocardial underperfusion during the interval of coronary vasodilation in the presence of a flow-limiting proximal coronary artery stenosis caused continuing subendocardial ischemia which resulted in augmentation of the reactive hyperemic response. In this experimental model both the redistribution of myocardial blood flow which occurred during an interval of restricted arterial inflow after a 5-s coronary artery occlusion and augmentation of the subsequent reactive hyperemic response were returned toward normal by nitroglycerin. This effect of nitroglycerin may have resulted, at least in part, from its ability to vasodilate the penetrating arteries which deliver blood from the epicardial surface to the subendocardium.
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PMID:Effects of nitroglycerin on transmural myocardial blood flow in the unanesthetized dog. 80 96

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

An experimental model of angina pectoris has been developed in order to study the hemodynamic, metabolic and electrophysiological alterations of the heart assumed to occur in the human disease and to analyze the influence of nitroglycerin and dipyridamole on the above changes. In anesthetized and thoractomized dogs, the left anterior descending coronary artery was autoperfused from the subclavian artery. Coronary blood flow was reduced until the epicardial monopolar electrocardiogram recorded from the myocardial segment supplied by the constricted coronary artery was just short of ischemic changes. O2 consumption and lactate uptake of the same segment were determined from the arteriovenous difference by sampling venous blood draining this area. Increasing heart rate by 50 to 70 beats/min by electrical pacing of the right atrium evoked a reversible and reporducible elevation of the ST segment and T wave of the electrocardiogram. Blood flow to the area perfused by the constricted coronary artery as well as the O2 uptake of the same area failed to increase on pacing. A concomitant decrease of lactate uptake, sometimes becoming even negative, was indicative of ischemia of that area. These changes could be reduced or prevented by a 10-minute infusion of a total dose of 20 mug/kg of nitroglycerin but not by 60 mug/kg of dipyridamole. Since the changes are fully reversible and readily reproducible, and the response also appears to show parallelisms with those observed in the human patient during an acute angina pectoris attack, use of this model for the assay of antianginal drugs seems to be warranted.
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PMID:Nitroglycerin and dipyridamole on cardiac metabolism and dynamics in a new experimental model of angina pectoris. 81 80

To determine the effect of isosorbide dinitrate or ischemic myocardium, this agent was administered to dogs with well developed coronary collateral vessels 8 to 14 weeks after embolization and subsequent occlusion of the left anterior descending coronary artery. After thoracotomy the left coronary artery was cannulated and perfused with blood from the femoral artery. The distal left anterior descending artery was cannulated to monitor peripheral coronary pressure. Regional contractile force in the normal left circumflex and potentially ischemic left anterior descending regions was measured with isometric strain gauge arches sewn to the epicardium. Moderate decreases in coronary perfusion pressure averaging 27 mm Hg produced selective ischemia in the myocardium beyond the site of occlusion of the left anterior descending artery. Under these conditions the average increase in peripheral coronary pressure produced by intracoronary injection of isosorbide dinitrate was 9.0 mm Hg, whereas contractile force in the ischemic region increased by 30 percent. The contractile force was unchanged in the normal regions. Therefore, isosorbide dinitrate can dilate coronary collateral vessels and improve contractile force in ischemic areas. Intracoronary injection of nitroglycerin had similar effects. The durations of responses to isosorbide dinitrate and nitroglycerin were remarkably similar: 6.4 and 6.7 minutes, respectively. Although isosorbide dinitrate can directly dilate coronary collateral vessels, its effects are not longer lasting than those of nitroglycerin.
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PMID:Comparative effects of nitroglycerin and isosorbide dinitrate on coronary collateral vessels and ischemic myocardium in dogs. 81 10

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

Myocardial metabolism had been studied in 54 patients with continuous sampling of arterial (A) and coronary sinus (CS) blood during 8- to 10-min periods of control in sinus rhythm, rapid atrial pacing and recovery. The results showed that 17 subjects were normal or had insignificant coronary artery disease (CAD; nonischemic group = NI); 37 patients had significant CAD (ischemic group = 1) and developed clinical, hemodynamic, and electrocardographic evidence of myocardial ischemia during pacing, characterized by angina, elevated left ventricular end-diastolic pressure, and depressed ST segments. During pacing-induced ischemia the following metabolic abnormalities were detected: (1) myocardial anaerobiosis indicated by lactate % uptake ((A-CS)/AS X 100) of -17.2 +/- 5.0% (mean +/- SE); (2) myocardial loss of K+ suggested by an A-CS difference of -0.25 +/- 0.08 mEq/liter (N=18); (3) small but significant loss of inorganic phosphorus (Pi) of -1.0 +/- 1.4% (N=18); and (4) elevation of CS blood creatine phosphokinase activity (N=5). These metabolic abnormalities were temporally related to the other manifestations of myocardial ischemia and were not seen in the NI; Lactate production and Pi loss occurred in 75 and 55% of the IG, respectively, suggesting that accelerated anaerobic glycolysis was the best indicator of myocardial ischemia in man. K+ loss was an unreliable index in this experimental situation, since tachycardia alone caused significant K+ egress from the heart. Lactate production and K+ loss were reduced by nitroglycerin, which abolished angina and improved hemodynamics and electrocardiographic manifestations. That these metabolic abnormalities were not observed in all 1 patients may have been related to methodology, the random distribution of CAD, and the fact that the chemical composition of the CS blood reflects the metabolic balance of both well oxygenated and ischemic areas of the myocardium.
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PMID:Metabolic indicators of myocardial ischemia in man. 120 71

In a randomized, cross-over, double-blind study, the effects of nifedipine were compared with those of diltiazem in 20 patients with severe stable angina pectoris and multivessel coronary artery disease treated with nitrates and beta-blockers. The comparison was performed by bicycle ergometry, clinical evaluation, and ambulatory 24-h ECG monitoring for 7-8 weeks. As compared with placebo, both nifedipine and diltiazem significantly reduced the daily number of anginal attacks and nitroglycerin consumption; prolonged exercise duration, time to 1-mm ST segment depression, and to onset of angina; and reduced the sum of ST segment depressions at maximal identical load in ergometry. In ambulatory ECG monitoring, only nifedipine significantly diminished the duration of asymptomatic ST segment depression as compared with placebo. Antianginal and antiischemic effects of nifedipine and diltiazem were similar. Both nifedipine and diltiazem significantly increased the effects of treatment with nitrates and beta-blockers. Administration of nifedipine was safer because at night diltiazem caused significant bradycardia despite careful titration of optimum doses of the drug. Although the maximum well-tolerated doses of conventional medication suppressed anginal symptoms in some patients, they did not abolish ischemia either at ergometry or in daily life.
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PMID:Effects of nifedipine and diltiazem on myocardial ischemia in patients with severe stable angina pectoris treated with nitrates and beta-blockers. 128 86


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