Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P less than .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V5 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.
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PMID:Indices of myocardial oxygenation during coronary-artery revascularization in man with morphine versus halothane anesthesia. 43 35

The effect of halothane on net myocardial oxygen balance of ischemic myocardium was studied in the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (sigma ST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 per cent) to six dogs with chloralose-urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P less than .001), heart rate (P less than .01), and the product of systolic arterial pressure X heart rate (P less than .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. sigmaST during occlusion was less (P less .001) during halothane (26.5 +/- 7.4 (SD) mv) than before (36.6 +/- 5.4 mv) or after (34.4 +/- 8.2 mv) its administration. Thus, halothane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.
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PMID:Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart. 96 78

Active vasoconstriction of epicardial coronary arteries can cause myocardial ischemia in patients with coronary artery disease. Relief of vasoconstriction can improve blood flow to the heart. The purpose of this study was to determine if 1.5 MAC halothane and 1.5 MAC isoflurane would each attenuate contractions evoked by three putative mediators of coronary constriction in coronary arteries removed from the hearts of human beings. Hearts were obtained in the operating room from five patients undergoing cardiac transplantation and from six brain-dead patients undergoing organ donation procedures. Coronary arteries were dissected free, cut into rings, and studied in organ chambers. Endothelium-dependent relaxations to 10(-6) M bradykinin were examined; they indicated a variable degree of endothelial dysfunction in vessels used in the experiments. Contractile responses to 40 mM KCl were tested and were used as control contractions. Contractions evoked by serotonin, histamine, and prostaglandin F2 alpha were measured and were expressed as a percent of contractile responses evoked by 40 mM KCl. Halothane depressed the agonist-induced contractions. Maximal contractile responses to serotonin were 130% +/- 28% in untreated rings and 63% +/- 10% in rings exposed to halothane (P less than 0.03). Responses to histamine were 183% +/- 46% untreated and 121% +/- 26% during halothane administration (P less than 0.05), and responses to prostaglandin F2 alpha were 227% +/- 42% untreated and 148% +/- 18% with halothane (P less than 0.05). Isoflurane had no effect on contractions. The results demonstrate that 1.5 MAC halothane, but not 1.5 MAC isoflurane, attenuates contractile responses evoked by putative mediators of coronary vasoconstriction in coronary arteries removed from the hearts of human beings.
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PMID:Halothane 1.5 MAC, isoflurane 1.5 MAC, and the contractile responses of coronary arteries obtained from human hearts. 200 36

Parameters of haemodynamic and myocardial oxygen supply under effect of 1.0-2.0 vol.% Halothane and Enfluran were studied under conditions of surgical stress in 12 patients with IHD of the III-IV functional classes. It was found out that the heart work and oxygen demand decreased in parallel to increase in dose of anesthetics and were adequately provided by the coronary blood flow. No signs of myocardial ischemia were determined.
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PMID:[Comparative evaluation of the effect of halothane and enflurane on the myocardial function and metabolism in patients with ischemic heart disease]. 342 25

This study was performed to test the hypothesis that halothane inhibits calcium accumulation associated with myocardial ischemia and calcium paradox. Using a Langendorff preparation in isolated guinea pig hearts, tissue 45Ca was measured after 40 and 60 min of loading with 45Ca, followed by 20 min of washout period. Myocardial ischemia was produced by a 30-min occlusion of the left anterior descending coronary artery (LAD). LAD occlusion caused an increase in 45Ca content in the anterior left ventricular muscle (ischemic area) of 215% compared to that of the posterior left ventricular muscle (normal myocardium). The increase in 45Ca content in the ischemic area was significantly less (P less than 0.05) in the presence of halothane (1%) compared to the non-halothane group. Halothane did not significantly alter 45Ca content in the non-ischemic myocardium. Myocardial injury associated with calcium paradox, which was produced by a 10-min perfusion of the heart with calcium-free Krebs solution followed by normal calcium repletion, caused a significant increase (P less than 0.05) in the 45Ca content compared to control. Addition of halothane (1%) significantly depressed (P less than 0.05) the increase in 45Ca content caused by calcium paradox. It is suggested that halothane might inhibit calcium accumulation associated with myocardial ischemia and calcium paradox under certain experimental situations. The inhibitory effect of halothane on calcium accumulation may be beneficial for the ischemic heart during halothane anesthesia.
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PMID:Halothane inhibits calcium accumulation following myocardial ischemia and calcium paradox in guinea pig hearts. 360 46

The effects of intravenous (iv) nifedipine (7.5 micrograms/kg over 10 min) on systemic hemodynamics and myocardial contractility were investigated under steady state conditions of halothane anesthesia (0.5 MAC) in 8 patients scheduled for elective coronary artery bypass surgery. All patients received long-term medication in the form of beta adrenergic receptor blockers and had a normal global left ventricular function at rest. Halothane produced a marked reduction in left ventricular contractility as documented by a considerable fall in LV max dP/dt. Nifedipine caused a small additional depression of LV max dP/dt without affecting LVEDP significantly. The slight myocardial depressant effect of nifedipine was counterbalanced by a concomitant reduction in left ventricular afterload due to a decrease in the systemic vascular resistance resulting in unchanged or even improved cardiac output. The results indicate that iv nifedipine in the doses used here is safe for patients with ischemic heart disease, even in the presence of already compromised myocardial contractility due to halothane anesthesia and chronic low-dose beta blocker therapy.
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PMID:Cardiovascular interactions of halothane anesthesia and nifedipine in patients subjected to elective coronary artery bypass surgery. 619 57

The interaction of halothane anesthesia and intravenous verapamil (0.15 mg/kg over 10 min) was investigated in eight patients scheduled for coronary artery bypass surgery. All patients had a normal left ventricular (LV) function at rest and were on chronic beta-blocker therapy. Halothane produced a marked reduction in mean arterial pressure (MAP), cardiac index, and in LV contractility as documented by a decrease in LV peak positive dP/dt. Verapamil caused an additional depression (16%) of LV peak positive dP/dt accompanied by a small increase (3 mm Hg) in LV end-diastolic pressure. The combined negative inotropic propensities of halothane and verapamil did not produce any overt untoward effects even in the presence of chronic low dose beta-blocker therapy. The predominant hemodynamic effect of verapamil was a systemic vasodilation resulting in a further reduction in MAP (12%) while heart rate remained unaffected. Despite reducing myocardial oxygen demand, caution must be exercised in dose selection in each drug to avoid regional myocardial ischemia due to the combined hypotensive effects of halothane and verapamil.
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PMID:Combined effects of halothane anesthesia and verapamil on systemic hemodynamics and left ventricular myocardial contractility in patients with ischemic heart disease. 633 75

Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodymanic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%) stoke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.
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PMID:Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischaemic heart disease and heart failure. 710 35

We studied the effect of halothane on regional myocardial function during acute ischemia and reperfusion in an open-chest pig model. Anesthesia was induced with thiopental and fentanyl and maintained with an intravenous (IV) infusion of pentobarbital and fentanyl. Regional myocardial function was studied with microsonometers placed in the subendocardium supplied by the left anterior descending coronary (LAD) and circumflex coronary artery (LX). Systolic function was evaluated with reference to the end-systolic pressure-length relationship (ESPLR) and regional systolic shortening. Diastolic dysfunction was studied with postsystolic shortening (PSS). Ischemia was induced with 15 min of total occlusion of the LAD artery, and thereafter reperfusion was allowed for 120 min. Five groups were studied: one group received only pentobarbital and fentanyl (n = 10); the other groups received halothane 0.2% (n = 5), 0.4% (n = 7), 0.6% (n = 5), and 0.8% (n = 5). The pentobarbital and fentanyl infusion was adjusted in the halothane groups in an effort to maintain arterial blood pressure and heart rate within specified limits (when possible). Results indicate that regional dysfunction during acute ischemia was equal among all the groups. However, on reperfusion, halothane significantly reduced the incidence of ventricular arrhythmias. Halothane (0.6% and 0.8%) was associated with less regional postischemic systolic dysfunction during reperfusion when compared to the other groups. Hearts subjected to 0.6% and 0.8% halothane also were less stiff at the end of systole (i.e., the extrapolated ventricular volume at zero ventricular pressure was less) after 120 min reperfusion compared to animals receiving less halothane. However, diastolic dysfunction was equal among the groups during reperfusion. We conclude that, in this model, administration of halothane is associated with improved recovery of regional systolic function and potentially beneficial pressure-length relations at the end of systole after acute severe myocardial ischemia and reperfusion. Furthermore, administration of halothane was associated with fewer reperfusion arrhythmias compared to animals not receiving halothane.
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PMID:Halothane and the reperfusion injury in the intact animal model. 846 9