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)

Acute coronary occlusion during PTCA represents a significant procedural complication occurring in approximately 4-5% of cases, most frequently because of coronary dissection, spasm, or thrombosis. In these cases the first step in the management of acute ischemia is 1) a brief evaluation of its hemodynamic consequences and 2) the assessment and treatment of its cause. Spasm and intracoronary thrombus formation are usually readily identifiable and treatable using intracoronary nitroglycerin and thrombolytic therapy. In our catheterization laboratory the current approach to occlusive coronary dissection is represented by the use of autoperfusion dilatation catheters and by stent application. The atherectomy devices and the laser "welding" of the dissected intimal segment represent other alternatives that are still under clinical evaluation in this particular setting. If coronary occlusion is refractory to these efforts and coronary blood flow is not reestablished rapidly, emergency coronary bypass surgery is required to salvage jeopardized myocardium. In this case myocardial ischemia may be lessened by the insertion of an intra-aortic balloon pump. In our experience, the incidence of death (4%) and myocardial infarction (37%) for emergency CABG after a failed angioplasty, is similar to that reported by other Authors. The duration of myocardial ischemia and the presence of cardiogenic shock before operation are the most important determinants of major complications such as death and acute myocardial infarction.
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PMID:[Surgical indications and results of myocardial revascularization in complications of PTCA]. 142 76

To assess the antiischemic efficacy of slow-release (SR) gallopamil, 100 mg b.i.d., versus slow-release (SR) nifedipine, 20 mg b.i.d., 24 patients with chronic stable angina underwent symptom-limited bicycle ergometer exercise stress tests in a randomized, placebo-controlled, double-blind, cross-over protocol. Both medications caused a significant reduction in anginal attack frequency and nitroglycerin consumption as compared to placebo; similarly, exercise tolerance was augmented in association with a considerable reduction in ischemia-induced ST-segment depression. The antiischemic effect of gallopamil (SR) was marginally superior to that of nifedipine (SR). Since the incidence of adverse effects was also less with gallopamil (SR) this drug exhibited a more favorable risk-benefit ratio relative to nifedipine (SR).
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PMID:[The anti-ischemic effect of gallopamil-retard in comparison with nifedipine-retard in stable angina pectoris]. 144 91

Four neonates had resolution of peripheral tissue ischemia after the application of 2% nitroglycerin ointment. A dosage of 4 mm nitroglycerin ointment per kilogram of body weight was applied to two patients with ischemia caused by vasospasm from indwelling radial artery catheterization and to two patients with ischemia resulting from dopamine extravasation. No adverse effects were noted except mild episodes of decreased blood pressure in two of the patients.
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PMID:Treatment of peripheral tissue ischemia with topical nitroglycerin ointment in neonates. 144 71

Acetylcholine (ACh) and nitroglycerin (NTG) were used as probes to study endothelium-dependent and endothelium-independent vascular relaxation in isolated perfused transverse paraumbilical human skin flaps. It was observed that ACh (10(-6) M) significantly (p < 0.05) decreased the vascular resistance and increased dermal capillary perfusion (assessed by surface fluorometry) in norepinephrine (NE, 10(-6) M) preconstricted skin flaps, despite the presence of a cyclooxygenase inhibitor (indomethacin, 3 x 10(-5) M) and a beta-adrenergic receptor antagonist (propranolol, 10(-6) M). The ability of ACh to induce vascular relaxation in NE-preconstricted skin flaps was lost after damaging the vascular endothelial lining with saponin perfusion (100 mg.L-1, 5 min). In contrast, NTG (10(-6) M) induced vascular relaxation to a similar extent before and after saponin treatment. In a separate study, ACh was seen to induce vascular relaxation in a concentration-dependent manner in skin flaps preconstricted with NE (10(-6) M). This vascular relaxation effect of ACh over the dose range of 10(-9)-10(-5) M was significantly (p < 0.01) inhibited in the presence of N omega-nitro-L-arginine (10(-5) M), a nitric oxide (NO) synthesis inhibitor. These observations were taken to indicate the presence of endothelium-dependent and endothelium-independent vascular relaxation in human skin flaps and that the ACh-induced endothelium-dependent relaxation is probably mediated by NO. The importance of impairment of endothelium-dependent relaxation in the pathogenesis of skin flap ischemia, and the potential use of topical nitrovasodilators or NO donors for prevention and (or) treatment of skin flap ischemia were also discussed.
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PMID:Evidence for endothelium-dependent and endothelium-independent vasodilation in human skin flaps. 149 89

Ischemia and reperfusion alter the reactivity of large coronary arteries, but the effect of ischemia and reperfusion on the coronary microcirculation has been less well defined. Elevated circulating levels of vasopressin are associated with cardiopulmonary bypass and numerous other clinical states in which vascular ischemia and reperfusion may occur. We examined the effects of ischemia with and without reperfusion on the responses to vasopressin of both large coronary arteries and coronary arterial microvessels. Studies were performed on vessels from control dogs (n = 8), dogs undergoing 1 hour of ischemia only (n = 8), and dogs undergoing 1 hour of ischemia followed with 1 hour of reperfusion (n = 9). Rings of proximal obtuse marginal coronary arteries distal to the site of circumflex coronary artery occlusion were studied in isolated organ chambers. Coronary microvessels (110 to 220 microns in diameter) were studied in a pressurized (20 mm Hg), no-flow state with a microvessel imaging apparatus and electronic dimension analyzer. Microvessels were preconstricted with the thromboxane A2 analog U46619. Responses of large vessel rings were studied in the nonpreconstricted state and after preconstriction with prostaglandin F2 alpha. Large vessel response to vasopressin was minimal and not altered by ischemia with or without reperfusion. In contrast, ischemia markedly affected the coronary microvascular response to vasopressin (10 to 1000 microU/ml). Control coronary microvessels constricted minimally to vasopressin (4% +/- 2% of the baseline diameter), while microvessels after either ischemia alone or ischemia followed by reperfusion constricted 22% +/- 5% and 21% +/- 3%, respectively (p less than 0.05 versus control for both). Hemoglobin, which inactivates the endothelium-derived relaxing factor, augmented microvascular constrictions to vasopressin in all groups to a similar extent. Relaxations to the endothelium-independent agent nitroglycerin were not altered by ischemia. Constrictions of the coronary microcirculation to vasopressin in conditions such as cardiopulmonary bypass or myocardial ischemia, in which circulating levels of vasopressin are increased, may predispose to persistent myocardial ischemia in the perioperative setting.
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PMID:Altered effects of vasopressin on the coronary circulation after ischemia. 149 97

Daily life ischemia has generated considerable interest because most of it is silent and associated with increased risk of adverse outcome. Coronary vasomotion, as well as increases in myocardial oxygen demand, seem important in the pathogenesis of this form of ischemia, so treatment with nitrates seems rational. Administration of sublingual nitroglycerin hourly, over 12 hours, was shown to decrease both silent and painful ischemic episodes in patients with effort angina. Subsequently, isosorbide dinitrate or mononitrate, given either as an intravenous infusion or orally, was shown to decrease both silent and painful ischemic episodes in patients with unstable rest angina and in those with severe angina. More recently, 6 studies have reported using transdermal nitroglycerin for daily life ischemia. Three of these reported open-label uncontrolled observations and suggested that ischemia frequency may be reduced approximately 60-80% during treatment with doses of 10-30 mg/day, with a duration of treatment ranging from 1 hour to 14 days. In 2 of these reports the duration of ischemia also decreased. The other 3 studies were randomized, double-blind, placebo-controlled studies with a total enrollment of 86 patients. These studies provided mixed results. One suggested that evidence for partial tolerance develops within 1 day of treatment, using large continuous or intermittent doses (mean, 52 mg/day). Another suggested that no tolerance develops to intermittent dosing (18 mg/16 hr out of 24 hr) during exercise testing but no effect is seen on daily life ischemia. The remaining study suggested that tolerance does not develop using small doses (15 mg/day) continuously over 14 days for ischemia during daily life, and that this response is different from that observed using the calcium antagonist nifedipine. These limited observations and conflicting results underscore a need for additional larger controlled trials, employing topical nitrate therapy in low intermittent doses for daily life ischemia.
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PMID:Daily life ischemia and nitrate therapy. 152 27

Hemodynamic changes were studied during two different anesthetic techniques in 54 patients undergoing coronary artery bypass grafting (CABG). All patients had normal to moderately impaired left ventricular function and were randomly assigned to two groups. In 27 patients, high thoracic epidural analgesia (TEA) with bupivacaine 0.375% plus sufentanil 1:200,000 (ie, 5 micrograms/mL) was used in combination with general anesthesia with midazolam/N2O; in the other 27 patients, general anesthesia (GA) with midazolam and sufentanil was used. After induction of epidural analgesia, heart rate and mean arterial pressure (MAP) decreased. Changes in cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure were not observed, whereas the stroke volume index increased significantly. After induction of intravenous anesthesia MAP decreased (20%) in both groups. During the pre-bypass period, metaraminol was used in 7 of 27 patients in the GA group and in 5 of 27 patients in the TEA group to treat hypotension. Inotopic drugs were used in 5 patients in the GA group and in none in the TEA group to treat a low CO. Ten GA patients and 4 TEA patients developed hypertension after sternal spread and the GA patients required more nitroprusside. Four GA patients developed electrocardiographic evidence of prebypass ischemia and, therefore, more nitroglycerin was needed for treating myocardial ischemia. More sodium nitroprusside was needed in the GA group during cardiopulmonary bypass (CPB) and the post-bypass period to treat hypertension with a high SVR. In conclusion, hemodynamic stability was more pronounced in the TEA than the GA group before and after CPB.
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PMID:Coronary artery bypass grafting using two different anesthetic techniques: Part I: Hemodynamic results. 847 38

Abnormalities of left ventricular (LV) systolic performance develop during exercise in patients with coronary artery disease (CAD) as a result of ischemia-induced regional wall motion abnormalities. Like patients with hypertension and those with hypertrophic cardiomyopathy, patients with CAD display abnormalities of LV diastolic performance under basal conditions in the absence of ischemia. The purpose of these studies was to compare the effects of bepridil versus those of propranolol or diltiazem in patients with exertional angina pectoris. LV systolic and diastolic performance were assessed at rest and during peak upright bicycle exercise by first-pass radionuclide ventriculography. Compared with propranolol, bepridil increased exercise capacity, cardiac output, and stroke volume and decreased systemic vascular resistance. Compared with diltiazem, bepridil increased exercise capacity, peak filling rate, and early diastolic filling fraction and decreased systemic vascular resistance, heart rate, time to peak filling rate, and atrial filling volume. Bepridil therapy is associated with improved exercise capacity and decreased anginal frequency and nitroglycerin consumption. In addition, its use is accompanied by favorable changes in LV systolic and diastolic function at rest and during exercise. These changes are consistent with benefits resulting from resolution of myocardial ischemia as well as from positive lusitropic effects of bepridil on the ventricular myocardium.
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PMID:Effects of antianginal therapy on left ventricular systolic and diastolic performance: comparison of the response to bepridil, propranolol, and diltiazem. 155 88

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

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.
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PMID:Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency. 157 47


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