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)

The effects of the stereoisomers of naloxone during myocardial ischemia were studied. (-)-Naloxone (but not the (+)-isomer naloxone) attenuated the ischemia-induced cardiac arrhythmias, hypotension, and bradycardia that result from coronary artery occlusion in anesthetized rats. From these findings, it may be inferred that endogenous opioid peptides may play a role in the pathophysiology of myocardial ischemia. It is also suggested that naloxone may have therapeutic value in the prevention and treatment of ischemic heart disease.
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PMID:Naloxone reversal of ischemic arrhythmia is stereospecific and suggests role of endogenous opioid peptides in ischemic heart disease. 150 43

Myocardial ischemia during surgery can be caused by coronary vasospasm. Neurohumoral mechanisms are involved in this phenomenon, and various substances have been suggested as possible causes, including acetylcholine, histamine, and norepinephrine. The responses of isolated porcine coronary arteries (from 117 pig hearts) with (E+) and without (E-) endothelium to these agents were investigated in the presence of fentanyl, sufentanil, and morphine. Fentanyl significantly shifted to the right, in a concentration-dependent fashion, the concentration-response curve to acetylcholine. This effect was not different between E+ and E- rings. Neither sufentanil nor morphine altered acetylcholine-induced contraction of porcine coronary arteries. Naloxone did not antagonize the suppressive effect of fentanyl on acetylcholine-induced contraction. The response of porcine coronary arteries to norepinephrine was decreased only at very high concentrations of fentanyl. Neither sufentanil nor morphine altered norepinephrine-induced contraction of porcine coronary arteries. Fentanyl, sufentanil, and morphine had no effect on histamine-induced contraction. We conclude that fentanyl antagonized acetylcholine-induced contraction of porcine coronary arteries. This effect of fentanyl seems to be caused by a direct effect on smooth muscle cells and is not opioid-receptor mediated.
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PMID:Effects of opioids on vasoresponsiveness of porcine coronary artery. 153 73

It was found, that injection of delta-receptors agonist dalargin before the occlusion of left anterior coronary artery in rats prevented the decrease of ventricular fibrillation threshold (VFT). An injection of naloxone in dose 0.5 mg/kg (for the blockade of mu-receptors only) had no influence on the VFT. Naloxone in dose 1 mg/kg (for the blockade peripheric mu- and delta-receptors) decreased VFT. An intraventricular infusion of dalargin (10 mkg) induced bradycardia and an increase of VFT. It was assumed that anti-arrhythmic effects of enkephalins in acute myocardial ischemia could be realized by an activation of peripheric delta-receptors and central mu-receptors.
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PMID:[Participation of central and peripheral mu- and delta opiate receptors in anti-arrhythmia action of enkephalins]. 166 48

An epidural catheter was inserted at T9-L2 interspace and 10 micrograms.kg-1 fentanyl with (E+) or without (E-) epinephrine 1:100,000 was given for 82 elective abdominal surgeries. N2O 66%, enflurane and muscle relaxant were used as needed. The onset and the duration of the action were estimated to be approximately 15 minutes and 4 hours, respectively. Anesthesia was maintained with enflurane below 0.4% (0.22 +/- 0.09%) in 70 patients (85.4%). E+ group needed significantly lower concentration of enflurane than E- group. There was no severe hemodynamic change during the operation. Systolic pressure, diastolic pressure and heart rate during the operation were 115.2 +/- 16.0 mmHg, 69.4 +/- 10.8 mmHg and 74.2 +/- 11.4 min-1, respectively, each of which was about 18% less than the values on arrival in the operating room. Sixty-one patients (82.5%) woke rapidly. Almost all patients felt well and had no pain during the recovery period. Naloxone 0.05-4 mg was administered intravenously in 21 patients (31.7%) whose respiratory rate was below 10 min-1. The patients with shorter operation time (shorter than 2.5 hours) needed more naloxone. Troubles of respiratory depression did not occur in the recovery room and in the ward in both naloxone and non-naloxone groups. This anesthesia method which induces mild depression of blood pressure and heart rate may be indicated for patients with ischemic heart disease or with poor cardiac function, but has no advantages in patients with poor respiratory function who need early extubation after a short operation.
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PMID:[Epidural anesthesia with high dose fentanyl for abdominal surgery]. 238 47

To determine whether endogenous opioids play a role in modulating the appreciation of chest pain in angina pectoris, the specific opioid antagonist, Naloxone, was used. The hypothesis was that the appearance time of ischemic myocardial pain should decrease after Naloxone if centrally mediated pain perception is significantly influenced by the endorphin system in angina pectoris. A randomized double blind clinical trial was conducted in 5 men with effort-induced angina pectoris associated with ST segment changes. Three multi-stage exercise tests, using the Bruce protocol were performed on the same day and time, on three successive weeks. Chest pain was reported 4.3 +/- 0.3 (SEM) minutes after starting exercise on the first or baseline test. On subsequent tests patients received either Naloxone 2 mg IV or a similar volume of saline placebo. Angina pectoris occurred significantly (p. less than 0.05) earlier (1.6 +/- 0.2 minutes) after Naloxone compared to placebo. There were no significant differences in myocardial ischemia indicated by ST segment changes and no significant differences in resting or exercise blood pressure and heart rate between Naloxone and placebo. Thus, these data focus attention on a neglected area of myocardial ischemic pain and suggest that endogenous opioids play a significant role in the recognition of the pain of effort-related angina pectoris.
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PMID:Effect of naloxone on exercise-induced angina pectoris: a randomized double blind crossover trial. 351 46

The effects of naloxone, propranolol, or both on the release of creatine kinase (CK) from the isolated ischemic rat heart were studied. Naloxone at concentrations of 1.1 and 3.6 mmole liter-1 in the perfusate at a rate of 1-2 ml min-1 reduced the release of CK from the isolated ischemic rat heart during myocardial ischemia in a dose-dependent manner. Propranolol at a concentration of 7 mumole liter-1 in the perfusate also reduced the release of CK. Addition of naloxone (1.1 mmole liter-1) to propranolol further reduced the release of CK. The effect of the joint administration of the two drugs seemed to be additive.
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PMID:Naloxone reduces release of creatine kinase in the isolated ischemic rat heart. 399 6

It has been demonstrated in experiments on rats that acute myocardial ischemia gives rise to a decrease in diuresis, elevation of antidiuretic activity of blood plasma and the blood concentration of immunoreactive aldosterone. Intraperitoneal injection of a synthetic enkephalin analog D-ala2-leu5-arg6-enkephalin in a dose of 1.25 nmol/kg bw resulted in partial normalization of diuresis, reduction in antidiuretic activity of blood plasma and blood aldosterone level to the control values. Naloxone eliminated the effects described. It is concluded that enkephalins have an inhibitory action on aldosterone and vasopressin secretion, with this action being mediated via opiate receptors.
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PMID:[Effect of enkephalins on vasopressin and aldosterone levels in acute experimental myocardial ischemia]. 646 18

Endorphins and endorphin receptors are believed to modulate pain perception. To investigate whether naloxone, a specific antagonist, could initiate anginal pain during exercise-induced myocardial ischemia in asymptomatic patients with angiographically defined coronary artery disease, a single-blind trial was conducted in 10 men with prior positive exercise electrocardiograms. Multistage treadmill exercise tests were performed twice within a week. On the second test, patients received naloxone, 2 mg intravenously, by a syringe infusion pump. Exercise was terminated because of fatigue in 6 patients and completion of the protocol in 4. No patient reported chest pain during exercise. Naloxone did not significantly alter exercise duration, heart rate, blood pressure and ST-segment changes compared with control testing. It is concluded that endorphins do not play a significant role in the recognition of anginal pain in patients who have asymptomatic exercise-induced ischemia.
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PMID:Naloxone and asymptomatic ischemia: failure to induce angina during exercise testing. 649 61

This investigation was to examine the effect of ferrous ion (a prooxidant) on the antiarrhythmic effect of naloxone (an endogenous opioid receptor antagonist) in isolated rat hearts. Isolated Sprague-Dawley rat hearts were perfused in the Langendorff mode and myocardial ischemia was performed by ligating the left descending coronary artery. Cardiac rhythm was recorded. Heart alpha-tocopherol concentrations were analyzed. Naloxone (1.2 micromol/heart) was effective in reducing the severity of arrhythmia (arrhythmia score; mean+/-S.E.M: 2.82+/-0.69 for naloxone vs. 5.18+/-0.38 for control, p<0.01). Fe2+ (100 nmol/heart) alone did not significantly affect the arrhythmia score (5.63+/-0.32) when compared with the control, however, Fe2+ administration did cause significant early onset of ventricular premature contraction and ventricular tachycardia. Additionally, Fe2+ administration diminished the naloxone's antiarrhythmic effect (arrhythmia score 4.12+/-0.40). Alpha-tocopherol, a major free radical scavenger that exerts protective functions on heart tissues during myocardial ischemia/reperfusion, was significantly higher in the naloxone-treated group (59.05+/-3.00 nmol/g wet wt) than in the control group (43.84+/-4.17 nmol/g wet wt, p<0.05). These results suggest that endogenous opioid peptides and reactive oxygen species might be related to ischemia-induced arrhythmia.
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PMID:Ferrous ion diminished the antiarrhythmic effect of naloxone in myocardial ischemia of isolated rat hearts. 970 54

The effects of myocardial ischemia and reperfusion on interstitial hydroxyl radical production, in the left ventricular myocardium of anesthetized cats, were investigated. Ringer's solution containing salicylic acid was perfused through an implanted microdialysis probe. Hydroxyl radical production was evaluated as the 2,3 and 2,5 dihydroxybenzoic acid (DHBA) concentrations in the microdialysates by an on-line high performance liquid chromatography system. Myocardial ischemia for 60 min, induced by ligation of the left anterior descending coronary artery, significantly increased both 2,3 and 2,5 DHBA levels when compared with the sham-operated cats. Naloxone (1 mg/kg, bolus, intravenous), an endogenous opioid peptide receptor antagonist, significantly suppressed the ischemia-induced production of hydroxyl radicals. Myocardial ischemia also induced cardiac arrhythmia. Naloxone reduced the severity of ischemia-induced arrhythmia, as observed by a significantly lower arrhythmia score (1.4 +/- 0.2 vs. 4.6 +/- 0.4 for control), and by diminished incidence of ventricular tachycardia (0/7 vs. 8/8 for control) and ventricular fibrillation (0/7 vs. 3/8 for control). Furthermore, perfusion of dynorphin (0.25 microgram, 2.5 micrograms and 25 micrograms), an endogenous opioid peptide receptor agonist, increased hydroxyl radical production. Our results suggest that, in anesthetized cats, myocardial ischemia can induce production of interstitial hydroxyl radical in left ventricular myocardium, and this production may involve the actions of released endogenous opioid peptides on their receptors.
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PMID:Increased formation of interstitial hydroxyl radical following myocardial ischemia: possible relationship to endogenous opioid peptides. 975 28


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