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)

The constant of elastance (E-MAX) is determined by measuring continuous left ventricular pressure and volume changes during the cardiac cycle. To evaluate the effect of myocardial ischemia on contractility, E-MAX was measured from serial pressure volume loops at baseline, with atrial pacing-induced ischemia, and after the administration of intravenous nitroglycerin with repeat pacing. Ten patients undergoing cardiac catheterization for presumed coronary artery disease were evaluated by this method. The severity of the coronary artery disease was graded angiographically by using the Gensini coronary score. In 8 of the 10 patients there was a significant decrease in E-MAX during atrial pacing (P less than .05). With the administration of nitroglycerin there was an attenuation of the ischemic effect previously noted with pacing. In 3 of the 10 patients administration of nitroglycerin produced a further decrease in E-MAX with ischemia. All 3 patients had a significantly lower Gensini coronary score with a well-developed, visible coronary collateral network. The authors' results indicate that continuous pressure volume loop analysis is possible using the nuclear stethoscope. Significant ischemic changes are seen with atrial pacing, which are relieved by the administration of nitroglycerin, except in the presence of coronary collaterals.
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PMID:Effect of ischemia on ventricular contractility in patients with coronary artery disease. 159 50

To test whether atrial natriuretic factor (ANF) may be involved in the modulation of coronary vasomotor tone, ANF was injected into angiographically normal left coronary arteries. Measurement of epicardial diameters of the circumflex (Cx) and left anterior descending artery (LAD) were made from biplane angiograms by an automatic contour-detection system. Bolus injection of ANF (0.07 micrograms/kg, diluted in 1 ml 0.9% NaCl, n = 7) increased diameter of proximal segments of LAD (11 +/- 4%) and Cx (10 +/- 4%) (p less than 0.02 each vs control) without altering heart rate and mean arterial pressure (MAP). Intracoronary nitroglycerin (NTG, 0.3 mg) increased diameters of identical LAD and Cx segments by 18 +/- 3% and 20 +/- 4%. Intracoronary ANF infusion (0.02 micrograms/kg/min over 5 min, followed by 0.1 micrograms/kg/min, n = 10) exerted dose-dependent increases in diameters of LAD and Cx (low dose: + 5 +/- 2%, p less than 0.05 vs control; high dose: + 13 +/- 3%, p less than 0.01 vs control). ANF-infusion increased arterial plasma ANF levels from 280 +/- 80 pg/ml during control to 894 +/- 82 pg/ml (low dose; + 614 pg/ml vs control) and to 2290 +/- 228 pg/ml (high dose). Severe ischemia in four patients undergoing angioplasty exerted substantial increase in arterial ANF levels (160 +/- 60 to 608 +/- 111 pg/ml; + 448 pg/ml vs control), similar to the increase elicited by low dose ANF infusion in man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of atrial natriuretic factor on coronary vascular tone]. 214 20

An acute ischemia has almost its origin in a mechanical obstruction of the vessel caused by embolus, thrombose or dissection. An ischemia caused by medicament, excepted the erronated intraarterial injection of vasoconstrictive medicament, is very seldom encountered in the clinic. We describe the case of a young woman who was referred to our clinic for investigation and treatment of an acute ischemia of both limbs. In her past medical history she was treated because of a liver insufficiency occurring after a spontaneous abortion and received methylergometrine (Methergin) for uterine stimulation. Because of this unusual manifestation in a young patient with a complicated past medical history we considered the possibility of a drug induced ischemia caused by ergotamine-derivate. The rapid recovering after treatment with chlorpromazine and nifedipine confirmed the suspected diagnosis. A well defined therapy of this rare complication has not been described; vasodilatators, nitroglycerin, calcium-antagonists and even streptokinase and balloon dilatation are proposed.
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PMID:[Drug-induced acute arterial occlusion]. 222 77

Isolated perfused rat hearts were subjected to global ischemia for 30 min followed by reperfusion for 2.5, 5, 10, or 20 min and then were tested for responsiveness to the endothelium-dependent vasodilator acetylcholine (ACh) and the endothelium-independent vasodilator nitroglycerin (NTG). ACh relaxation was impaired 2.5 min after reperfusion (32 +/- 3% of initial control, P less than 0.01) and remained comparably depressed at every time thereafter. No significant decrease in vasodilator response to NTG occurred at any time. Endothelial dysfunction was prevented by recombinant human superoxide dismutase (hSOD, 5 mg/heart) but not by the hydroxyl radical scavenger N-(2-mercaptopropionyl)-glycine (8 mg/heart). Comparable effects and a similar time course were observed in hypoxic hearts reoxygenated for periods up to 20 min. Chemiluminescence of perfusion effluent employed as an index of free radical production was measured at all postreperfusion times in ischemic hearts. Ischemia alone produced small increases in chemiluminescence. Reperfusion, however, produced significantly higher increases in chemiluminescence, with a large burst of activity at 0.25 min, which was blocked by hSOD. These findings suggest that endothelial dysfunction resulting in decreased release of endothelium-derived relaxing factor occurs very early after reperfusion or reoxygenation and may be due to the action of superoxide free radicals.
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PMID:Time course and mechanism of endothelial dysfunction in isolated ischemic- and hypoxic-perfused rat hearts. 226 Jun 93

Anesthesia-induced coronary vasospasm has been reported only rarely. We report a case, without previous cardiac history, in which immediately after anesthesia induction a marked ST elevation was noted on the EKG monitor. Premature ventricular contractions as well as non-sustained ventricular tachycardia were noted. These changes resolved immediately after nitroglycerin infusion and 75 mg of lidocaine were given. A coronary angiogram revealed normal coronary arteries and left ventriculogram. Ergonovine stimulation was not performed. The patient was discharged home on calcium entry blockers and nitrates. Exercise stress test two weeks after discharge was negative for ischemia. Induction of anesthesia triggering coronary spasm has been reported rarely, and to our knowledge never in the presence of angiographically normal coronary anatomy. Coronary vasospasm with typical EKG changes--namely, ST elevation and ventricular arrhythmias--has to be included as a possible complication of general anesthesia. Recognition of this syndrome allows prompt treatment and prevention of future episodes.
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PMID:Coronary artery spasm induced by anesthesia: a case report and review of the literature. 229 59

We examined the effects of ischemia with and without reperfusion on endothelium-dependent and -independent vascular relaxation in both conduit and resistance coronary arteries. Studies were performed on dogs under control conditions (n = 13) or after 1 hour of circumflex coronary artery occlusion with (n = 10) or without (n = 8) 1 hour of reperfusion. Rings of obtuse marginal branches of the left circumflex coronary artery (conduit arteries) were studied in organ chambers. Coronary microvessels (110-220-microns diameter) were studied in a pressurized state with an in vitro microvessel imaging apparatus. Relaxation was evaluated after preconstriction with prostaglandin F2 alpha and U46619 (a thromboxane A2 analogue) in conduit and resistance vessels, respectively. Conduit vessel function was not altered by ischemia with or without reperfusion. Endothelium-dependent microvascular relaxation was depressed in response to acetylcholine, ADP, and calcium ionophore A23187 after ischemia with reperfusion compared with control relaxation (ED50 as -log[M]: 6.0 +/- 0.2 [p less than 0.05], 5.1 +/- 0.4 [p less than 0.05], and 5.8 +/- 0.1 versus 6.8 +/- 0.2, 6.8 +/- 0.2, and 6.6 +/- 0.2, respectively). Ischemia without reperfusion modestly altered microvascular endothelium-dependent relaxation. Microvascular relaxation to nitroglycerin was not altered by ischemia with reperfusion. We conclude that 1) endothelium-dependent relaxation in large epicardial coronary arteries is relatively refractory to ischemia with or without reperfusion, 2) ischemia alone produces mild alterations of coronary microvascular reactivity, 3) ischemia followed by reperfusion produces a marked and selective impairment of endothelium-dependent responses in the coronary microcirculation.
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PMID:Ischemia-reperfusion impairs endothelium-dependent relaxation of coronary microvessels but does not affect large arteries. 237 5

The purpose of this study was to compare the effects of nicorandil [SG-75; 2-nicotinamidoethyl nitrate (ester)] and nitroglycerin on the distribution of blood flow between subendocardium and subepicardium [endocardial/epicardial blood flow ration (endo/epi)] distal to a proximal flow-limiting coronary artery stenosis in anesthetized dogs. Myocardial blood flow distribution was determined by use of 15-micron radioactive microspheres. Various indices of reactive hyperemia (peak flow, duration, volume) and poststenotic coronary pressures were used to assess the severity of ischemia in the area distal to the stenosis. Partial ischemia was produced by a 10-s total left circumflex coronary occlusion followed by 110 s of reflow to 50-60% of the control flow. Microspheres were injected during steady-state conditions during the partial reflow period. In the absence of drug, coronary artery stenosis produced marked underperfusion of the subendocardium (endo/epi, 0.55 +/- 0.05). Following administration of nicorandil (60 micrograms/kg i.v.) or nitroglycerin (15 micrograms/kg i.v.), the endo-epi during a subsequent partial reflow (stenosis present) period was significantly increased (0.67 +/- 0.06). The duration of reactive hyperemia and reactive hyperemic flow were also decreased by both compounds following release of the stenosis. These results suggest that nicorandil and nitroglycerin reduce subendocardial ischemia distal to a flow-limiting coronary artery stenosis. This beneficial effect may partially explain the efficacy of these two compounds in the therapy of angina pectoris.
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PMID:Enhanced subendocardial perfusion distal to a flow-limiting coronary artery stenosis in dogs: comparative effects of nicorandil, a potential new antianginal agent, and nitroglycerin. 241 11

To investigate the antianginal action of nitroglycerin and nifedipine, systemic and right heart pressures, cardiac output, oxygen consumption, and radionuclide left ventricular ejection fraction and volume were measured in 14 men with stable effort angina and a positive exercise electrocardiogram. Exercise tests were performed on a semiupright bicycle ergometer on no therapy and after intravenous nitroglycerin and sublingual nifedipine, which lowered mean arterial pressure by 20 mm Hg. Exercise tolerance improved from 50 +/- 4 to 61 +/- 5 W on nifedipine and to 79 +/- 4 W on nitroglycerin (p less than 0.01, nitroglycerin vs. nifedipine). At submaximal workloads, both drugs decreased arterial pressure and ventricular volumes, but heart rate was higher on nifedipine. At peak exercise on nitroglycerin (79 W), oxygen consumption, cardiac index, heart rate, and rate-pressure product were significantly increased over peak control and nifedipine values, while systolic pressure and end-diastolic volume were unchanged. Nitroglycerin reduced pulmonary wedge pressure more and systemic diastolic pressure less than nifedipine, so the coronary perfusion gradient was reduced by nifedipine and maintained by nitroglycerin. Also, there was less angina and ST-segment depression after nitroglycerin compared to control or nifedipine, and the left ventricular diastolic pressure-volume relationship was improved only by nitroglycerin. This suggests that the action of nitroglycerin in reducing ischemia is not only due to reduced myocardial oxygen demand, but that myocardial oxygen delivery may also be increased.
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PMID:Comparison of the effects of nifedipine and nitroglycerin on hemodynamic determinants of myocardial oxygen consumption and supply during exertional angina. 247 80

Symptom-limited exercise testing (SLET) makes it possible to appraise in a reproducible manner both the extent of ischemia and the circulatory profile. Therefore, repeated SLET with either one or another drug, or a combination of both allows a proper comparison and avoids the quite impractical trials lasting several weeks, far too complicated in the case of combination of drugs. From the knowledge of the components of myocardial oxygen demand and of the pharmacological properties of different drugs, it is easy to predict what combinations will be complementary, harmful, or redundant. The application of these principles to the individual patient is made easier by the determination of the circulatory profile and of the severity of ischemia. From that, the logical proposal for whichever combination is obvious. The more effective and less costly combination appears to be the association of beta 1-selective blockers and preventive sublingual nitroglycerin. beta-Blockers and nifedipine and diltiazem and molsidomine are also effective and well tolerated.
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PMID:Mono- or combination therapy for stable angina pectoris. 248 Nov 68

To investigate the antiischemic efficacy and development of tolerance to transdermal nitroglycerin, 14 patients with chronic, stable angina pectoris were studied using continuous ambulatory electrocardiographic monitoring. Patients demonstrated initial hemodynamic responsiveness to sublingual nitroglycerin and were titrated to a maximally tolerated dose of 30 to 60 mg/24 hours (52 +/- 5 mg). Two crossover phases were use in a randomized, double-blind, placebo-controlled manner: continuous nitroglycerin therapy (patches containing active drug worn for 24 hours) and intermittent nitroglycerin therapy (12-hour active drug followed by a 12-hour nitrate-free period). There were no differences in frequency or duration of ischemic episodes between the placebo days of each phase. A significant effect in frequency of episodes was observed between placebo and treatment days of continuous therapy (p less than 0.05). Nonsignificant reductions in frequency and duration of ischemic episodes also occurred during intermittent therapy. The major antiischemic effect of transdermal nitroglycerin therapy occurred during the first day of treatment but was lost by 48 hours. Reductions in frequency and duration of ischemic episodes (p less than 0.05) were present on day 1 of continuous therapy but ischemic episodes returned to placebo levels by day 2, suggesting the development of tolerance. Intermittent therapy did not prevent the development of tolerance on day 2 of treatment. The results demonstrate that the use of high doses of transdermal nitroglycerin in patients with chronic, stable coronary artery disease produced a beneficial reduction in the frequency and duration of ischemia. However, the antiischemic benefit was lost between 24 nd 48 hours after the onset of continuous and intermittent therapy, presumably due to tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dosing intervals on the development of tolerance to high dose transdermal nitroglycerin. 210 35


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