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)

Endothelial dysfunction, as evidenced by decreased stimulated release of endothelium-derived relaxing factor (EDRF), occurs after reperfusion of the ischemic myocardium. To better understand this endothelial dysfunction, isolated cat hearts were perfused under constant flow by the Langendorff procedure with Krebs-Henseleit solution devoid of blood cells. Following global ischemia (90 minutes) and reperfusion (20 minutes), coronary vasorelaxation to the endothelium-dependent vasodilator acetylcholine (ACh) was 70 +/- 3% of initial values (p less than 0.01) compared with 90 +/- 4% in nonischemic control perfused hearts. No decrement occurred in response to the endothelium-independent vasodilator nitroglycerin (NTG). Coronary artery rings isolated from the ischemic left circumflex coronary artery showed a similar degree of endothelial dysfunction to ACh, with normal relaxation in response to NaNO2. Autologous cat neutrophils (100 million cells), activated with 100 nmol/L f-met-leu-phe infused into the heart directly before and throughout reperfusion, resulted in a further decrement in ACh-induced vasodilation, to 55 +/- 5% of initial response, with no effect on NTG-induced vasodilation. Similar results were obtained with coronary artery rings isolated from perfused cat hearts and exposed to neutrophils. This neutrophil-enhanced endothelial dysfunction was inhibited by human superoxide dismutase as well as by an antibody to the adherence glycoprotein complex CD-18 (i.e., MAbR 15.7). Therefore endothelial dysfunction occurs initially upon reperfusion of the previously ischemic heart and is aggravated by superoxide radicals produced by activated neutrophils.
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PMID:Activated neutrophils aggravate endothelial dysfunction after reperfusion of the ischemic feline myocardium. 824 14

Endothelium-dependent relaxation of conductance coronary vessels involves nitric oxide formation from L-arginine. The present study examines whether a similar mechanism intervenes in the vasomotor control of resistance coronary vessels. In conscious dogs, the excess of coronary blood flow (CBF) created by intracoronary acetylcholine (3.0 ng/kg) averaged 7.2 +/- 1.1 ml. Intracoronary adenosine (100 ng/kg) increased CBF by 12.4 +/- 1.4 ml. Intracoronary nitroglycerin (175 ng/kg) increased CBF by 7.4 +/- 1.2 ml. CBF repayment-to-debt ratio after a 15-s coronary arterial occlusion averaged 2.8 +/- 0.2. After an intracoronary N omega-nitro-L-arginine dose (10 micrograms.kg-1.min-1 x 12 min) was given to inhibit nitric oxide formation, baseline CBF was not altered. CBF increases with acetylcholine averaged 2.4 +/- 0.5 and 6.4 +/- 0.7 ml with adenosine, both less (P less than 0.01) than responses before the arginine analogue. CBF increases with nitroglycerin averaged 7.2 +/- 1.1 ml, similar to control responses. CBF repayment-to-debt ratio during reactive hyperemic responses fell (P less than 0.01) to 1.7 +/- 0.1. L-Arginine (1.0 mg.kg-1.min-1 x 12 min) partially reversed the inhibitory effect of the arginine analogue on CBF responses to acetylcholine. Thus nitric oxide formed in resistance coronary vessels is a major mediator of coronary vasodilation to acetylcholine, adenosine and transient ischemia.
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PMID:Contribution of nitric oxide to dilation of resistance coronary vessels in conscious dogs. 173 2

The immediate and delayed effects of urokinase and heparin on minimal cross-sectional area of a patent ischemia-producing coronary artery were prospectively investigated in 43 patients with unstable angina. After baseline angiography, patients were randomized to 3 different treatment groups: group I--urokinase (1,000,000 U intravenous bolus dose), followed by heparin infusion 3 hours later; group II--heparin (10,000 U intravenous bolus, followed by continuous infusion); and group III--conventional therapy only (intravenous nitroglycerin, beta blockers and calcium antagonists). Angiography was repeated at 1 hour and at 8 days of treatment and minimal cross-sectional area was determined in the 35 patients who completed the study. In group I, minimal cross-sectional area increased from 0.84 +/- 0.48 mm2 at baseline to 0.94 +/- 0.49 mm2 at 1 hour (p less than 0.05), and to 1.00 +/- 0.51 mm2 at 8 days (p less than 0.01 vs baseline). In group II, a significant increase in minimal cross-sectional area was observed only at the 8-day angiography (0.64 +/- 0.39 mm2 at baseline; 0.67 +/- 0.37 mm2 at 1 hour [p = not significant]; and 0.79 +/- 0.48 mm2 at 8 days [p less than 0.01] vs baseline). In group III, no significant changes in minimal cross-sectional area occurred either at 1 hour or at 8 days. Thus, both urokinase and heparin improved lesion geometry in patients with unstable angina, although a large individual variation was noticed. The effect occurred earlier with urokinase than with heparin.
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PMID:Effects of urokinase and heparin on minimal cross-sectional area of the culprit narrowing in unstable angina pectoris. 187 70

Blood cardioplegia at 8 degrees C results in cardiac standstill whilst maintaining minimal metabolic functions of the cardiac cell. Reinjection every 20 minutes allows cellular reoxygenation, the delivery of essential elements (Tham, CPD), and the elimination of products of myocardial degradation accumulated during ischemia. Before declamping the aorta, a reperfusion with warm blood (34 degrees C) containing glutamate and GTN enables restocking of the energy reserves (Krebs' cycle) and a lowering of coronary and systemic resistances. This technique used systematically if even more effective when the ischemic time is prolonged as is the case in cardiac transplantation. The 50 transplants performed since January 1989 with this form of myocardial protection were compared with 50 procedures performed in 1988 with crystalloid cardioplegia. There was no significant difference in the duration of ischemia or of cardiopulmonary bypass between the two groups. Patients benefitting from blood cardioplegia defibrillated spontaneously more frequently, required lower doses of Dopamine for shorter periods and were extubated earlier.
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PMID:[Value of the association of blood cardioplegia and energetic warm reperfusion in cardiac transplantation]. 189 13

A noninfarcted, entirely collateral-dependent myocardial region provides an opportunity to assess the effect of nitroglycerin on coronary collateral function during exercise. Stress thallium-201 computed tomography was performed in seven patients with effort angina and no history of myocardial infarction, both before and after nitroglycerin (0.3 mg). All patients had single-vessel disease with total or subtotal (99% with delay) occlusion of proximal left anterior descending coronary artery and well-developed collaterals. The pressure-rate product, mean blood pressure, and heart rate at peak exercise did not differ before and after nitroglycerin. The size of the perfusion defect and the severity of ischemia during exercise estimated by quantitative analysis of thallium-201 single photon emission computed tomography were significantly less after nitroglycerin administration (extent score: 23 +/- 17 vs 7 +/- 9, p less than 0.01; severity score: 20 +/- 22 vs 3 +/- 4, p less than 0.05). The pressure-rate products at peak exercise did not differ before and after nitroglycerin, which suggested that the reduction in perfusion defect size was unlikely to be the result of decreased myocardial oxygen consumption. These results suggest that nitroglycerin improved coronary collateral function during exercise and thus prevented exercise-induced myocardial ischemia.
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PMID:Effect of nitroglycerin on coronary collateral function during exercise evaluated by quantitative analysis of thallium-201 single photon emission computed tomography. 190 51

To examine the effect of initial coronary reperfusion pressure on endothelial function, we subjected 16 isolated perfused neonatal lamb hearts to 2 hours of ischemia with potassium cardioplegic solution followed by reperfusion for 1 hour. Before ischemia both acetylcholine, an endothelium-dependent vasodilator, and nitroglycerin, and endothelium-independent vasodilator, caused coronary vasodilation. After ischemia the response to acetylcholine was impaired in the eight hearts with high initial reperfusion pressure (60 mm Hg) but was intact in the eight hearts with low initial reperfusion pressure (20 mm Hg for 10 minutes, 40 mm Hg for 10 minutes, and then 60 mm Hg thereafter). The response to nitroglycerin, however, remained intact regardless of initial reperfusion pressure. Recovery of resting coronary flow and myocardial oxygen consumption was lower in the group with high pressure reperfusion than in the group with low pressure reperfusion. On reperfusion a transient burst of coronary flow was exhibited by the hearts reperfused at high pressure. These results suggest that high initial reperfusion pressure impairs the endothelial modulation of coronary tone; this may be related to the effects on the coronary vasculature of the "burst" of coronary flow associated with high intravascular pressure.
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PMID:Influence of initial reperfusion pressure after hypothermic cardioplegic ischemia on endothelial modulation of coronary tone in neonatal lambs. Impaired coronary vasodilator response to acetylcholine. 190 38

The purpose of this study was to determine if intraarterial vasodilating drugs could augment the vasodilation produced by sympathetic blockade, such as occurs during epidural anesthesia. Papaverine (2 mg/min), nitroglycerin (1 microgram/kg/min), aand saline were infused into the femoral artery before and after lumbar sympathectomy in six arterially isolated canine hindlimbs. Femoral blood flow was controlled with a perfusion circuit at baseline (80 ml/min), half-baseline (40 ml/min), and low (5 ml/min) flow rates so that hindlimb mean arterial pressure served as an index of peripheral vasodilation. At low flow, hindlimb arteriovenous oxygen content difference increased from 1.4 (baseline) to 6.2 ml O2/dl, consistent with peripheral ischemia. At baseline flow before sympathectomy, papaverine and nitroglycerin caused a decrease in hindlimb mean arterial pressure of 30% and 18%, respectively (p less than 0.01 vs saline control), equivalent to the decreases of 31% and 16% after sympathectomy (p less than 0.01). At half-baseline, papaverine and nitroglycerin reduced hindlimb mean arterial pressure by 22% and 12%, respectively (p less than 0.01), and caused comparable vasodilation after sympathectomy. Neither drug significantly changed hindlimb mean arterial pressure at low flow. Sympathectomy itself reduced hindlimb mean arterial pressure by 23% at baseline flow (p less than 0.01), by 18% at half-baseline flow (p less than 0.01), but had no effect at low flow. We conclude that intraarterial papaverine and nitroglycerin cause peripheral vasodilation that is synergistic with sympathectomy-induced adrenergic blockade, but they cannot augment vasodilation caused by peripheral ischemia.
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PMID:The interaction of vasodilating drugs and sympathetic blockade in normal and ischemic canine hindlimbs. 190 19

The antianginal efficacy of metoprolol OROS has been investigated in comparison with that of atenolol in a multicenter double-blind cross-over trial carried out in patients with stable effort angina. OROS (ORally OSmotic) is a new semi-permeable delivery system with very slow osmotic release of the active drug, which is maintained at virtually constant plasma levels throughout the 24 hours. At the end of a 2-week run-in period, 53 patients with chronic coronary artery disease and documented ischemia during bicycleergometric exercise test were given, on double-blind condition, metoprolol OROS 21/285 and atenolol 100 mg in random order for 4 weeks each. On the last day of each cross-over period, patients underwent a bicycleergometric exercise test 24 hours after the last drug intake. The mean number of anginal attacks (2.54 during the 2-week run-in period) decreased under both metoprolol OROS (1.29 and 1.13 after 2 and 4 weeks of treatment, respectively) and atenolol (1.29 and 0.73 after 2 and 4 weeks of treatment, respectively), with no difference between the two beta-blockers. The same behaviour was observed as regards the nitroglycerin tablets consumption. The exercise test variables (i.e. duration of exercise, maximum workload and peak exercise values of systolic and diastolic blood pressure, heart rate and ST-segment depression) did not differ between the two treatments and did not show a time-effect. The percentage of patients reporting adverse effects was low with both treatments. Two patients were withdrawn from the study during atenolol (gastralgia and heartburn, respectively), and one during metoprolol OROS (gastralgia).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of metoprolol OROS with antenolol in the treatment of effort angina pectoris: a randomized double-blind study. 190 34

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

The systemic hemodynamic and coronary dilative responses to sublingual nitroglycerin were studied in patients receiving transdermal nitroglycerin. A total of 48 patients with coronary artery disease were divided into 4 groups: 12 patients receiving 1 tablet of sublingual nitroglycerin without transdermal nitroglycerin (Group 1), 12 patients receiving 1 tablet of sublingual nitroglycerin with 12-hour-daily intermittent therapy of transdermal nitroglycerin (Group 2), 12 patients receiving 1 tablet of sublingual nitroglycerin with continuous therapy of transdermal nitroglycerin with continuous therapy of transdermal nitroglycerin (Group 3), and 12 patients receiving 2 tablets of sublingual nitroglycerin with continuous therapy of transdermal nitroglycerin (Group 4). Before and during administration of sublingual nitroglycerin, aortic pressure, left ventricular pressure, and coronary artery diameter were examined at diagnostic cardiac catheterization in all patients. During sublingual nitroglycerin, the decreases of aortic systolic pressure and left ventricular end-diastolic pressure were greater in Group 1, 2, and 4 than in Group 3. Dilation of coronary arteries by sublingual nitroglycerin tended to be greater in Group 1, 2, and 4 than in Group 3. Thus, the effects of sublingual nitroglycerin for the relief of ischemia might be more prominent in patients with intermittent therapy of transdermal nitroglycerin than in those with continuous therapy. The increased dose of sublingual nitroglycerin for the relief of ischemia might be more effective in patients with continuous therapy of transdermal nitroglycerin.
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PMID:Effects of sublingual nitroglycerin in patients receiving transdermal nitroglycerin for coronary artery disease: prevention of cross-tolerance. 191 67


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