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)

Coronary artery surgery, the preferred technique for myocardial revascularization in patients with ischemic heart disease, promptly increases blood flow to areas of the myocardium distal to the coronary obstruction. CAS completely relieves angina in 90% of patients. The risk of 1 to 5% is decreasing as operative technique and patient selection improve. Patients having CAS need comprehensive preoperative and discharge teaching to restore them to normal, active, optimistic lives.
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PMID:Coronary artery surgery. Operative technique and patient education. 17 67

Efficacy and safety of two different dose regimens of isosorbide-5-mononitrate (isosorbide mononitrate, ISMN, Mono Mack, CAS 16051-77-7) (40 mg ISMN in the morning, n = 187 vs. 20 mg ISMN b.i.d. morning and early afternoon, n = 195) were evaluated in an open, randomised study in patients with symptomatic myocardial ischemia. Circadian rate, frequency, severity and duration of angina pectoris attacks, as well as the additional need of short-acting nitrates were assessed on 3 consecutive days before and at the end of the first and second weeks of treatment, respectively. In both treatment groups, a statistically significant decrease of frequency and severity of angina pectoris attacks was observed as compared to baseline. Apart from minor variations, no statistically significant differences were found between the two treatment groups.
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PMID:Influence of isosorbide-5-mononitrate on the circadian rhythm of angina pectoris. 149 89

The effect of KW-3635 (sodium (E)-11-[2-(5,6-dimethyl-1-benzimidazolyl) ethylidene]-6,11-dihydrodibenz[b,e] oxepine-2-carboxylate monohydrate, CAS 127166-41-0), a novel thromboxane A2 (TxA2) receptor antagonist, on collagen-induced coronary ischemia was studied in guinea-pigs. Under pentobarbital anaesthesia, intravenous injection (i.v.) of collagen (1 mg/kg) induced abnormal ECG changes such as ST-T changes, elevation of T-wave arrhythmia and cardiac arrest in severe cases. The changes of ECG (leads I, II and III) were recorded for 10 min following collagen injection. KW-3635 (25-50 mg/kg p.o.) remarkably improved the collagen-induced ischemic ECG changes. The effect of KW-3635 was more potent than those of daltroban, isbogrel and ticlopidine. Neither nifedipine nor propranolol had any effect. The plasma thromboxane B2 level in the KW-3635-treated animals was lower in comparison with those in both the control and daltroban-treated animals. These results suggest that TxA2 may play a role in this model of coronary ischemia and that KW-3635 is effective in the treatment of ischemic heart disease.
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PMID:Beneficial effect of the novel thromboxane A2 receptor antagonist sodium (E)-11-[2-(5,6-dimethyl-1-benzimidazolyl)ethylidene]-6,11- dihydrodibenz[b,e]oxepine-2-carboxylate monohydrate on collagen-induced coronary ischemia in guinea-pigs. 181 24

Calcium (Ca) agonists like Bay k 8644 ((-)-S-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl) pyridine-5-carboxylate (CAS 93468-89-4), may represent a new principle in the treatment of heart failure. Because of marked vasoconstrictive properties, these agents may have a deleterious effect on myocardial ischemia (MI). It was however demonstrated that contractility enhancement and coronary flow (CF) reduction do not automatically enlarge MI. Therefore, we investigated the influence of Bay k 8644 (10(-8) mol/l) in comparison to ouabain (1.5 x 10(-7) mol/l) in non-arrhythmogenic concentrations on MI in electrically paced isolated rabbit hearts (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca2+ 1.8 mmol/l, 180 beats/min). MI was induced by coronary artery ligation and quantified by epicardial NADH-fluorescence. Left ventricular pressure (LVP) was significantly increased by ouabain (+10-20%) but slightly diminished by Bay k 8644 (-10%) (p < 0.05). CF reduction after Bay k 8644 (-30%) was more pronounced than after ouabain (-10%) (p < 0.05), but both substances did reduce relative CF (CF/LVP x heart rate) to the same extent (-20-30%) (p > 0.05). Nevertheless, ouabain did not significantly influence epicardial NADH-fluorescence area or intensity (p > 0.05), whereas MI was significantly enlarged by Bay k 8644 (+30%) (p < 0.05). It is concluded that in isolated rabbit hearts ouabain and Bay k 8644 might influence CF-distribution differently with a more pronounced diminuation of the nutritive CF induced by Bay k 8644.
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PMID:Influence of dihydropyridine-type calcium agonists on hemodynamics and myocardial ischemia in isolated rabbit hearts. 750 84

In the present study a novel nitric oxide (NO) donor, CAS-1609, was utilized as a means of coronary NO replenishment in a canine model of myocardial ischemia-reperfusion. Administration of CAS-1609 (1.25 mg iv) 10 min before reperfusion, followed by a 1 mg/h intracoronary infusion throughout the 4.5-h reperfusion period, resulted in significant improvement in postischemic transmural myocardial blood flow (0.66 +/- 0.09 vs. 0.37 +/- 0.08 ml.min-1.g-1 for saline vehicle, P < 0.05). Dogs receiving NO supplementation also exhibited a significant recovery of myocardial contractility after 4.5 h of reperfusion (30 +/- 2% area ejection fraction vs. 22 +/- 2% for saline vehicle, P < 0.05). Moreover, myocardial necrosis as a percentage of the area at risk was reduced from 28.9 +/- 4.3% in the saline group to 8.5 +/- 2.6% in the CAS-1609 group (P < 0.01), while ischemic zone myeloperoxidase activity, indicative of neutrophil infiltration, was also attenuated by 70% with NO therapy. Injection of acetylcholine and nitroglycerin into the left circumflex coronary artery revealed a significant impairment of vasodilator responses in the saline vehicle dogs at 2 h of reperfusion. However, dogs treated with the NO donor demonstrated postischemic vasodilator responses which were similar to baseline (P = not significant vs. baseline). These studies demonstrate that intracoronary administration of NO significantly augments postischemic coronary blood flow and contractile function following ischemia and reperfusion. In addition, NO therapy reduces coronary vascular injury, attenuates myocardial necrosis, and reduces neutrophil infiltration. The cardioprotective actions of intracoronary NO administration may be related to the potent antineutrophil actions of NO.
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PMID:Intracoronary nitric oxide improves postischemic coronary blood flow and myocardial contractile function. 757 9

Antianginal effects of monatepil ([(+-)-N-(6,11-dihydrodibenzo[b,e]thiepin-11-yl)-4-(4-fluor ophenyl)-1-piperazinebutanamide]monomaleate, AJ-2615, CAS 10337-41-9), a new calcium antagonist, were evaluated in experimentally induced myocardial ischemia in anesthetized rats and compared with those of diltiazem. Ischemic electrocardiogram change (ST elevation) and reduction of myocardial tissue oxygen tension were induced by intracoronary arterial administration of U-46619 ((5Z,9a,11a,13E,15(S))-9,11-(methano-epoxy)prosta-5,13-di en-1-oic acid) (10 micrograms/kg), a stable thromboxane A2 agonist. The ST elevation induced by U-46619 was significantly prevented by monatepil pretreatment (0.1 mg/kg i.v.), and to a lesser extent by diltiazem (0.3 mg/kg i.v.). Moreover, the decrease in myocardial tissue oxygen tension at the time of ST elevation after U-46619 was inhibited by monatepil pretreatment (0.3 mg/kg i.v.). These results indicate that monatepil exerts a more potent preventive effect against U-46619-induced myocardial ischemic changes than diltiazem and suggest that monatepil has potential for treating vasospastic angina.
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PMID:Preventive effect of monatepil on thromboxane A2 agonist-induced myocardial ischemia in rats. 805 69

Ascorbic acid (CAS 50-81-7) might mediate cardioprotective effects by scavenging free oxygen radicals. The effects of exogenous ascorbic acid on acute myocardial ischemia (MI) was investigated in isolated electrically-driven rabbit hearts (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca2+ 1.8 mmol/l, 37 degrees C). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature and quantitated from epicardial NADH-fluorescence photography. Starting after a reperfusion period of 20 min, isolated hearts were treated with ascorbic acid (10(-5) or 10(-4) mol/l). Ascorbic acid had no significant influence on the left ventricular left ventricular pressure or the coronary flow (p > 0.05). Ascorbic acid had no significant effect on epicardial NADH-fluorescence area or intensity (p > 0.05). Free radical scavenging properties reported for ascorbic acid do not mediate cardioprotective effects at the concentrations used in isolated rabbit hearts.
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PMID:Studies of the cardioprotective effects of ascorbic acid in isolated rabbit hearts. 985 Apr 28

The abilities of 2-(2-methylphenyl)-5,7-dimethoxy-4-quinolyl carbonylguanidine dihydrochloride (CAS 181048-29-3, MS-31-050) and 2-phenyl-8-(2-methoxyethoxy)-4-quinolyl carbonylguanidine bismethanesulfonate (CAS 181048-36-2, MS-31-038) in inhibiting Na(+)-H+ exchange, ischemia- and reperfusion-induced injury were determined and compared with those of 4-isopropyl-3-methylsulfonylbenzoyl guanidine methanesulfonate (CAS 159138-81-5, IMGM), a selective inhibitor of Na(+)-H+ exchange. MS-31-050 and IMGM exhibited comparable inhibitory effects on Na(+)-dependent pH recovery and antiarrhythmic effects during ischemia in anesthetized rats. In rats subjected to ischemia and reperfusion, MS-31-050 (10 mg/kg i.v.) significantly reduced the infarct size when given prior to the onset of ischemia. However, postischemic treatment with either MS-31-050 or IMGM failed to protect reperfused hearts. In contrast, MS-31-038 reduced the infarct size dramatically from 65.4 +/- 7.4% in control to 29.9 +/- 11.6% at 3 mg/kg and 9.8 +/- 3.4% at 10 mg/kg even when administered before the onset of reperfusion. These results suggest the beneficial effects of Na(+)-H+ exchange inhibitors on myocardial ischemia/reperfusion injury.
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PMID:Effects of MS-31-038, a novel Na(+)-H+ exchange inhibitor, on the myocardial infarct size in rats after postischemic administration. 1033 48

In this study, the model of early myocardial infarction (EMI) was produced by legation of left anterior descending artery in rat. The artery spasm (CAS) was produced by external jugular vein injection of vasopressin (VP). Myocardium of apex and adjoining slice was used to make paraffin sections, then HE and LSAB-Mb staining were performed. Results showed: In 25 min after myocardial infarction, stretch-shape Mb depletion was observed in subendocardial myocardium of aortic ventricle's frontal wall. As the time of EMI prolonged, stretch-shape Mb depletion extended to epicardial layer. In CAS group, multiply, spotty Mb depletion was detected. There were more Mb depletion zones in right heart than that in left heart. The Mb depletion zones surrounded the CA or were like grape-clusters along the branches of one large CA. Thus, myocardial Mb depletion induced by EMI and CAS had different morphologic peculiarity. LSAB-Mb method could be hoped for the use of supplying objectively morphologic evidence to myocardial ischemia induced by CAS.
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PMID:[Experimental study of myocardial myoglobin depletion induced by early myocardial infarction and coronary artery spasm]. 1037 22

In the present study a series of trimetazidine (1-(2,3,4-trimethoxybenzyl)piperazine, CAS 5011-34-7) derivatives is subjected to quantitative structure-activity relationship (QSAR) analysis aiming at establishing the relationship between molecular structure and the binding affinity of the compounds to the respective receptor sites in the cells. Trimetazidine is used in the therapy of ischaemic heart disease. Literature data for the biological effect of the compounds are used. The derivatives studied include compounds with different substituents at the fourth position of the piperazine ring and a variation between the ortho-methoxy and ortho-hydroxy group in the benzyl residue. A statistically significant correlation between the Van der Waals volume of the substituents and the binding affinity of the respective compounds was found.
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PMID:Quantitative structure-activity relationship analysis of the substituent effects on the binding affinity of derivatives of trimetazidine. 1497 3


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