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)

Thromboxane A2 (TxA2) has been implicated as a mediator of ischemic damage to the myocardium. A new, selective thromboxane receptor antagonist, SQ-29,548 (2 mg/kg bolus + 2 mg/kg per h infusion) was studied for its effects on the extension of ischemic damage following acute myocardial ischemia (MI) in the rat. Administration of SQ-29,548 to sham MI rats had no significant effect on mean arterial blood pressure or heart rate over the 6 h experimental protocol. Ischemic damage was assessed by measurement of the depletion of creatine kinase (CK) activity and amino-nitrogen concentration from the myocardium. Six hours following ligation of the left main coronary artery, there was a significant loss of both CK (P less than 0.001) and amino-nitrogen (P less than 0.001) from the left ventricular free wall (LVFW). Administration of SQ-29,548 significantly blunted this loss of CK activity (P less than 0.01) and amino-nitrogen concentration (P less than 0.001) from the ischemic myocardium. Furthermore, the survival rate at 6 h following acute coronary artery ligation was 100% (7/7) for rats given SQ-29,548 and 58% (11/19) for rats given only the vehicle (P less than 0.05). These data indicate that SQ-29,548 significantly prevents the extension of ischemic damage in the myocardium and improves survival following acute coronary artery ligation, suggesting an important role for TxA2 in the pathophysiology of acute myocardial ischemia.
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PMID:Anti-ischemic actions of a new thromboxane receptor antagonist, SQ-29,548, in acute myocardial ischemia. 301 42

Common electrocardiographic manifestations (CEM) are predictors of ischemic heart disease (IHD). If precursors of the disease, their risk factors should be similar to those of IHD. This hypothesis has been assessed on results of multiphasic screening recorded in 1976 and 1981, in 1,347 45-65 year old men. Risk factors are social class (blue collar relative risk rr = 2.3), physical activity at work (sedentariness rr = 2.4), systolic blood pressure, no beer consumption and blood urea nitrogen with an exponential risk curve. Cholesterolemia, smoking, diabetes mellitus, overweight and uricemia are not predictors of CEM incidence within 5 years. These results support the idea that CEM are partially asymptomatic expression of IHD; they also have another significance. Subgroups should be individualized and analysis yielded on larger samples. Correlation analysis has been performed between IHD mortality and beer consumption on basis of French counties. A positive correlation (r = 62, p less than 0.01) is opposed to individual results.
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PMID:[Epidemiology of minor electrocardiographic anomalies predictive of the occurrence of ischemic cardiopathy]. 310 84

The role of platelet activating factor (PAF) in acute myocardial ischemia (MI), produced by the ligation of the left main coronary artery, was studied in anesthetized rats. A significant loss of cardiac amino-nitrogen concentration and cathepsin D activity was observed 6 hr after permanent occlusion MI or 10 min of MI followed by 6 hr of reperfusion in rats. A novel, potent, PAF antagonist, CV-6209 (160 nmol/kg or 1.6 mumol/kg) injected after the ligation, significantly retarded the loss of amino-nitrogen and cathepsin D activity in a dose-related manner. In another group of rats, CV-6209 (1.6 mumol/kg) significantly blocked the hypotension induced by repetitive injections of PAF (570 pmol/kg) with an apparent half-life of approximately 180 min. In isolated rat hearts perfused with Krebs-Henseleit solution, PAF (25 nmol/l) significantly increased coronary perfusion pressure by 15 +/- 2 mmHg and induced an increase in cardiac permeability using fluorescein isothiocyanate bovine albumin as a marker. Furthermore, the increase in cardiac permeability induced in isolated perfused rat hearts undergoing 15 min global ischemia followed by reperfusion was significantly attenuated by CV-6209 (250 nmol/l). These data indicate that PAF is an important mediator of ischemic damage in rat MI. Moreover, the extension of ischemic damage may be enhanced by the increase in cardiac permeability induced by PAF.
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PMID:Role of platelet activating factor in propagation of cardiac damage during myocardial ischemia. 325 36

The role of hypertension and antihypertensive drugs in cardiovascular complications was evaluated in 380 elderly people living in the Tokyo Metropolitan Gerontology Center. The subjects were classified into four groups according to the presence or absence of hypertension and their antihypertensive treatment, and followed up prospectively for 5 years from 1979 to 1984. The average age of each group was 74 to 76 years. Cerebrovascular disease was observed in 19.3% of male hypertensives and 10.1% of male normotensives (p = 0.078). The drug treated group revealed no cerebral hemorrhage and less cerebral infarction. This tendency was not observed in females. Ischemic heart disease was prevalent in the drug treated group (10.9% vs 4.5%, p = 0.023) irrespective of blood pressure level. Risk factors such as body mass index, skinfold thickness, serum cholesterol, albumin, creatinine, blood urea nitrogen and uric acid at entry were elevated in the drug treated group. Diuretics were used in 92% of the drug treated group; in 53% as monotherapy and in 39% as combination therapy with other antihypertensive agents. The metabolic effect of diuretics may increase the incidence of ischemic heart disease in the elderly. We might conclude that hypertension in the aged accelerates cerebrovascular complications, and that antihypertensive treatment is effective even in this group. However, the wide use of diuretics could increase the incidence of ischemic heart disease. Careful selection of antihypertensive drugs as well as dose adjustment are needed in the treatment of elderly hypertensives.
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PMID:Effects of hypertension and antihypertensive drugs on cardiovascular complications in the elderly. 336 87

Although nitrous oxide is commonly administered to patients with ischemic heart disease, recent reports suggest that it may induce myocardial ischemia in these patients. The authors compared the effects of nitrous oxide on segmental left ventricular (LV) function and the ST segment of the electrocardiogram with the effects of an equal concentration of nitrogen (crossover design) before the start of surgery in 18 patients who required coronary-artery bypass grafting. The patients studied did not have valvular or LV dysfunction. Anesthesia was induced and maintained with intravenous fentanyl. After endotracheal intubation and 20 min of ventilation with 100% oxygen, either 60% nitrous oxide or 60% nitrogen (randomly assigned) was added to the inspired gas mixture of each patient for 10 min. This was followed by 10 min of 100% oxygen, and then 10 min of 60% nitrous oxide or 60% nitrogen, whichever had not been administered previously. Patients were monitored for myocardial ischemia using a standard 12-lead electrocardiogram and trans-esophageal two-dimensional echocardiography. Surgery did not begin until the study was concluded. No patient experienced an ST segment change greater than 1 mm during the study, and none developed a new segmental wall motion abnormality during inhalation of either nitrous oxide or nitrogen. The authors conclude that nitrous oxide does not induce myocardial ischemia when used as an adjunct to fentanyl anesthesia in patients who have severe coronary-artery disease accompanied by well-preserved valvular and LV function.
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PMID:Addition of nitrous oxide to fentanyl anesthesia does not induce myocardial ischemia in patients with ischemic heart disease. 368 36

We investigated the effects of acute myocardial ischemia (MI) in a rabbit model of atherosclerosis to determine whether atherosclerosis augments the severity of damage produced in the ischemic myocardium. Normal rabbits were fed a control rabbit chow diet or a diet enriched with either 2% cholesterol or 0.5% cholesterol for 10-12 weeks prior to induction of MI. Plasma cholesterol concentrations in the cholesterol-fed rabbits were 1697 +/- 70 mg/dl (2%) and 1056 +/- 51 mg/dl (0.5%) vs. 61 +/- 12 mg/dl for the non-cholesterol-fed rabbits. All rabbits were observed for 5 h following induction of MI or sham MI. At the conclusion of the experiment, tissue biopsies from the MI region and non-MI (NMI) regions were taken and analyzed for two indicators of the severity of MI--myocardial creatine kinase (CK) activity and free amino-nitrogen concentration. Atherosclerosis was confirmed histologically in coronary artery and aortic specimens. No difference was found among any group with respect to heart rate (HR), mean arterial blood pressure (MABP), or pressure-rate index (HR x MABP/1000, a measure of myocardial oxygen demand). Myocardial CK loss (NMI - MI) was significantly greater for the 2% and 0.5% cholesterol groups (7.3 +/- 1.3 and 4.9 +/- 0.7 IU/mg protein, respectively, P less than 0.05) than in the nonatherosclerotic group (2.5 +/- 0.4 IU/mg protein; P less than 0.001 for 2% and P less than 0.01 for 0.5%). Increased severity of MI was confirmed by a significantly greater myocardial loss of free amino-nitrogen (NMI - MI) in the two atherosclerotic groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased severity of acute myocardial ischemia in experimental atherosclerosis. 369 58

U-63,557A, a new selective thromboxane synthetase inhibitor, was evaluated for its ability to prevent the extension of myocardial infarct size. Left coronary arteries of male Sprague-Dawley rats (230 - 270 g) were acutely ligated, producing a consistent model of myocardial infarction (MI) in rats analyzed 48 hours later. Left ventricular free wall (LVFW), creatine kinase (CK) activity, and amino-nitrogen concentrations were assayed as indices of infarct size. U-63,557A was administered intravenously in two doses (4 and 8 mg/kg) with a split schedule (2 min post-ischemia and either 4 or 24 hrs later). Administration of the thromboxane synthetase inhibitor significantly reduced both myocardial CK and amino-nitrogen loss at a dose of 8 mg/kg, but it was only slightly effective at 4 mg/kg. Drug treatment significantly increased the percent LVFW spared; 27 +/- 3% (vehicle) vs 43 +/- 7% and 52 +/- 7% (8 mg/kg). U-63,557A is an effective agent in myocardial ischemia for limiting the extension of infarct size after acute coronary artery ligation. Previous studies of other thromboxane synthetase inhibitors showed effectiveness in the early stages of MI. This study shows an effect on true infarct size 48 hours post-ligation, and suggests that inhibition of thromboxane A2 plays an important role in the pathogenesis of ischemic damage in the myocardium.
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PMID:Protective action of a thromboxane synthetase inhibitor in preventing extension of infarct size in acute myocardial infarction. 385 43

Products of the lipoxygenase pathway of arachidonate metabolism, including hydroperoxides, free radicals, and leukotrienes, are thought to mediate ischemic damage during acute myocardial ischemia (MI). Propyl gallate (1 mg/kg/h) was infused in anesthetized cats 0.5 h after coronary artery occlusion. Propyl gallate did not influence mean arterial blood pressure (MABP), heart rate (HR), or the product of these, the pressure-rate index. Treatment of MI with propyl gallate significantly reduced the plasma accumulation of creatine kinase (CK). This was confirmed by reduced CK loss in biopsies from the ischemic region of the heart, indicative of a protective effect. Propyl gallate also reduced the loss of compounds containing amino-nitrogen groups from the ischemic region, although it did not significantly reverse the S-T segment elevation in the electrocardiogram. These results are consistent with the concept that inhibition of formation of lipoxygenase products protects the myocardium from ischemic damage. This study also helps explain the work of others demonstrating that combined cyclooxygenase-lipoxygenase inhibitors or depletion of leukocytes is beneficial in MI.
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PMID:Protective actions of propyl gallate, a lipoxygenase inhibitor, on the ischemic myocardium. 391 59

A specific inhibitor of thromboxane A2 (TxA2) synthesis, CGS-13080, was studied during acute myocardial ischemia (MI) in cats. To define more clearly the mechanism of action of CGS-13080, we also studied it effects on isolated cat coronary arteries, in vitro aggregation of cat platelets, and production of thromboxane B2 (TxB2) from cat platelet-rich plasma (PRP). MI cats that received the vehicle for CGS-13080 exhibited a significant increase in plasma concentration of TxB2. This was accompanied by increases in the ST segment of the electrocardiogram, specific activity of plasma creatine kinase (CK), and loss of CK activity and amino-nitrogen from the ischemic myocardium. In contrast, TxB2 concentrations, plasma and tissue CK activities, and myocardial amino-nitrogen concentration of MI cats treated with CGS-13080 were not significantly different from those in sham MI cats that had received the drug. In vitro, CGS-13080 did not inhibit contraction of cat coronary arteries produced by a stable TxA2 analog and did not inhibit aggregation of cat PRP indiced by arachidonic acid (AA). However, production of TxB2 by cat platelets treated with AA was completely inhibited by this agent. Thus, specific inhibition of TxA2 synthesis without thromboxane receptor antagonism can exert a protective effect on the myocardium during ischemia in cats.
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PMID:Protection of ischemic cat myocardium by CGS-13080, a selective potent thromboxane A2 synthesis inhibitor. 619 74

Enalapril, a new potent orally active angiotensin-converting enzyme inhibitor, was studied in cats subjected to acute myocardial ischemia. Enalapril, administered intravenously (2 mg/kg, plus 2 mg/kg/h) 30 min after ligation of the left coronary artery, significantly reduced the pressure-rate index, an indicator of myocardial oxygen demand. This was confirmed in isolated cat papillary muscles where enalapril reduced contractile force by 5-10%. During myocardial ischemia, enalapril reversed the elevated S-T segment of the electrocardiogram toward normal 2 h after the onset of ischemia. Moreover, enalapril significantly blunted the increases in circulating creatine kinase (CK) activity, as well as significantly prevented the loss in myocardial CK activity. These changes correlated with reduced myocardial loss of compounds containing free amino-nitrogen. Enalapril effectively acted as a converting enzyme inhibitor over the 5-hour course of the observation period. However, enalapril also acted as an angiotensin antagonist in isolated coronary arteries, a finding that may help explain its efficacy in myocardial ischemia. Enalapril did not appear to stabilize the membranes of cat liver lysosomes, and thus probably does not protect the ischemic myocardium by lysosomal stabilization.
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PMID:Cardioprotective effects of enalapril in acute myocardial ischemia. 620 18


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