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)

In previous experiments on dogs subjected to local myocardial ischemia, we have shown a late and prolonged anti-ischemic and anti-arrhythmic effect of a single injection of the stable prostacyclin analogue, 7-oxo-PgI2. The protection was dependent on dose and time. Maximal effects were observed 48 hours after an optimal intramuscular dose of 50/micrograms/kg. To study the mechanism of this protective effect we have followed the time-dependent changes in transmembrane cation homeostasis induced by ischemia and reperfusion by measuring the intracellular potassium, sodium and calcium ion concentrations in Langendorff guinea pig heart preparations isolated from untreated control animals and from animals receiving a single intramuscular injection of 50/micrograms/kg 7-oxo-PgI2 48 hours before preparation. Global ischemia was produced by stopping perfusion for 25 minutes and was followed by reperfusion. In a second series, similarly treated and untreated hearts were fixed for electron microscopy after 25 minutes' global ischemia as well as after 15 minutes' reperfusion. Ischemia and reperfusion evoked a rapid loss of intracellular potassium and gain of sodium as well as an accumulation of calcium in the reperfusion phase. Pretreatment with 7-oxo-PgI2 prevented all these changes. It also prevented the shortening of the sarcomers and swelling of mitochondria induced by ischemia and the deposition of calcium-dense granules in mitochondria appearing after reperfusion. The findings support the hypothesis that 7-oxo-PgI2 has a delayed cytoprotective action which preserves normal transmembrane ion transport and normal structure of myocardial cells under conditions of ischemic and reperfusion injury.
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PMID:Delayed protection by 7-oxo-PGI2 against cardiac transmembrane ion shifts and early morphological changes due to ischemia and reperfusion. 210 94

The effects of acidified sodium nitrite (NaNO2) which releases nitric oxide, a substance which is thought to be indistinguishable from endothelium-derived relaxing factor, were investigated in a 6-h model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. Acidified NaNO2 (12.5-50 mmol/kg/hr) was infused i.v., starting 30 min postocclusion followed by reperfusion 1 hr later, in cats subjected to MI by occlusion of the left anterior descending coronary artery. Acidified NaNO2 infusion (25 and 50 mmol/kg/hr) resulted in significantly lower plasma creatine kinase activities at every time beyond 1 hr for the MI + vehicle group, and was not significantly different when compared to sham MI + NaNO2 controls. The areas at risk expressed as percentage of the total left ventricular weights were not significantly different between the MI + vehicle and MI + acidified NaNO2 groups. However, the necrotic area expressed as a percentage of the myocardial area at risk was significantly lower in the 25 and 50 mmol/kg/hr NaNO2-treated cats. Cardiac myeloperoxidase activities indicated that significantly fewer neutrophils were attracted to the ischemic zone of the NaNO2-treated MI cats when compared to the vehicle-infused MI cats. Acidified NaNO2 significantly inhibited platelet aggregation in a dose-dependent manner in cat platelet-rich plasma. Thus, acidified NaNO2 exerts a significant protective action during ischemia and reperfusion injury, which suggests that endothelium-derived relaxing factor has a cardioprotective effect in MI.
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PMID:Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion. 215 7

We compared the effects of myocardial ischemia and postmortem changes on beta-adrenergic receptors and their coupling to adenylate cyclase activity. The effects of 1 h of left circumflex coronary artery occlusion were examined in eight conscious calves, which were then anesthetized with pentobarbital sodium, and the left ventricle was divided into nonischemic and ischemic regions. A crude membrane fraction was prepared from each region and from the nonischemic tissue 1 h postmortem. beta-Adrenergic receptor density increased (152 +/- 55%) and decreases in basal (-21 +/- 6.1%), isoproterenol-stimulated (-25 +/- 8.0%), 5'-guanylylimidodiphosphate [Gpp(NH)p]-stimulated (-17 +/- 5.8%), fluoride-stimulated (-26 +/- 5.8%), and forskolin-stimulated (-31 +/- 8.4%) adenylate cyclase activities were observed in the ischemic myocardium compared with nonischemic myocardium. Similarly, in postmortem samples, beta-adrenergic receptor density rose 58 +/- 16%, whereas decreases in basal (-48 +/- 8.7%), isoproterenol-stimulated (-61 +/- 7.8%), Gpp(NH)p-stimulated (-58 +/- 7.0%), fluoride-stimulated (-64 +/- 6.1%), and forskolin-stimulated (-52 +/- 6.2%) adenylate cyclase activities were observed. Agonist-binding competition curves with isoproterenol were shifted, indicating that beta-adrenergic receptors were binding agonists with low affinity in both the ischemic and postmortem myocardium. The marked, but directionally opposite, changes in receptor density and adenylate cyclase that occur postmortem indicate the importance of prompt processing of tissues. The striking similarity in response of beta-adrenergic receptor agonist and antagonist binding and adenylate cyclase activity in ischemic and postmortem tissue raises the speculation that similar mechanisms may operate under both conditions.
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PMID:Beta-receptors and adenylate cyclase: comparison of nonischemic, ischemic, and postmortem tissue. 215 29

The effects of acidified sodium nitrite (NaNO2), a releaser of nitric oxide (NO), combined with human superoxide dismutase (hSOD), were investigated in a 6-hour model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. Acidified NaNO2 (12.5 mmol/kg/hr) was infused intravenously in cats starting 0.5 hour after occlusion of the left anterior descending (LAD) coronary artery, which was reperfused 1.5 hour following occlusion. Significantly lower plasma creatine phosphokinase activities were observed at all times beyond 3 hours for MI cats given NaNO2 + hSOD when compared with the other MI groups. The areas-at-risk expressed as percentages of the total left ventricular weights were not significantly different among any of the MI groups. However, the necrotic area expressed as a percentage of the myocardial area-at-risk was significantly lower in the MI + NaNO2 + hSOD-treated cats compared with all other MI groups. The NaNO2-treated group also produced a significant decrease in the necrotic area relative to the area-at-risk. Cardiac myeloperoxidase (MPO) activities indicated no significant difference in number of neutrophils attracted to the ischemic zone in the NaNO2 + hSOD-treated MI cats when compared with the other MI groups. Acidified NaNO2 + hSOD together exert significant protection on the myocardium subjected to ischemia and reperfusion injury. NaNO2 may act synergistically with hSOD to prolong the action of NO by scavenging free radicals that inactivate NO.
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PMID:Synergism between superoxide dismutase and sodium nitrite in cardioprotection following ischemia and reperfusion. 215 21

Today it is accepted that estrogens mitigate the consequences of ischemic heart disease. Preliminary experiments revealed an increase in heart sarcolemmal (Na+ + K+)-ATPase activity after application of estradiol in vivo. It is also well known the key role of latter enzyme for heart function. The facts mentioned above indicate that estradiol may act on the heart just via modulation of the (Na+ + K+)-ATPase activity. In present paper it is confirmed that 17-beta-estradiol stimulates the activity of sarcolemmal (Na+ + K+)-ATPase by allosteric manner, particularly by increasing positive cooperativity between the K(+)-binding sites of the enzyme. This effect is manifested by enhancement in functional capacity of the sodium pump in sarcolemma. Stimulatory effect of estradiol is bound to integrated myocytes: neither is it manifested in isolated sarcolemma in vitro nor exhibits any influence on the affinity of binding sites for cardiac glycosides or on total capacity of the sarcolemma to bind ouabain. Basing on the data obtained it was assumed that estradiol acts on the (Na+ + K+)-ATPase not directly but by means of a mediator released within the myocyte.
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PMID:Mechanism of action of estradiol on sodium pump in sarcolemma from the myocardium. 217 17

The concentration of C peptide which is an indicator of the secretory capacity of the beta-cells of the pancreas was assessed in 109 patients with type II diabetes, hospitalized on account of prolonged difficulties as regards compensation. The values on fasting, the maximal values after stimulation following an experimental meal and increments were greater than in age- and weight-matched controls. In diabetic patients some highly significant relationships were revealed between the C peptide concentration on fasting and indicators of the risk of ischaemic heart disease [IHD]. They included HDL cholesterol, the body mass index and uric acid. The relationship between the maximal C peptide concentration and serum sodium may be associated with a greater disposition for hypertension. Thirty-one patients with symptoms of an ischaemic myocardial lesion had a significantly elevated C peptide concentration on fasting. The increments of C peptide concentration after an alimentary stimulus correlated indirectly with indicators of the actual and long-term compensation of diabetes. In relation to the reduced increments also the need of insulin therapy was reflected. Data obtained by examination of the C peptide concentration in the blood of type II diabetics can contribute to the objectivization of needs of insulin treatment and to the detection of the link between cardiovascular risk and hyperinulinaemia.
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PMID:[The importance of C-peptide determination in the treatment and prognosis of type II diabetes]. 218 36

Racial differences in the prevalence, course, and pathophysiologic characteristics of hypertension in black and white populations are reviewed. Accumulated epidemiologic data indicate that the prevalence of hypertension among blacks is greater than that among whites in almost all age- and sex-matched groups. Hypertensive blacks have a higher incidence of left ventricular dysfunction, stroke, and renal damage, but a lower incidence of ischemic heart disease, than do hypertensive whites. A significant pathophysiologic difference between blacks and whites is salt sensitivity; normotensive, as well as hypertensive, blacks tend to be salt sensitive. Blacks also tend to have lower renin levels than do whites, while dopamine response to a salt load is diminished among blacks as compared with whites. These differences and others lead to the recommendation that hypertension among blacks should be managed initially with salt restriction; if dietary control is insufficient, administration of an antihypertensive agent with 24-hour efficacy, which lowers vascular peripheral resistance, promotes sodium excretion, and potentially improves renal hemodynamics, is recommended. A calcium channel blocker may satisfy these requirements.
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PMID:Hypertension: racial differences. 222 Jul 99

Endoscopic variceal sclerotherapy (EVS) is an effective means of controlling variceal hemorrhage, which develops as a consequence of portal hypertension. While esophageal perforation, ulceration, strictures, and mediastinitis are potential complications associated with this procedure, it is not clear whether isolated pleuropulmonary events such as pleuritis, pneumonitis, and adult respiratory distress syndrome are causally related to the EVS. Endoscopy and sedation with the attendant risk of aspiration, particularly in the background of hepatic encephalopathy, may account for some of these events. Recent controlled studies of respiratory function demonstrate that EVS as such results in minor changes in gas exchange, lung volumes, and pulmonary and systemic hemodynamics. Most pulmonary complications have been reported with the use of sodium morrhuate sclerosant. Comparative studies among different sclerosants are necessary to evaluate relative safety. Finally, there have been rare reports of myocardial ischemia and pericarditis reported in association with EVS, but these are of a transient nature. Chest symptoms, roentgenographic pleuropulmonary changes, pulmonary hemodynamics, and cardiac perturbations are transient and should not preclude offering EVS to patients with variceal hemorrhage.
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PMID:Cardiorespiratory effects of endoscopic esophageal variceal sclerotherapy. 222 Aug 81

The following discourse addresses the pharmacologic profile of KT-362, its clinical potential as an anti-arrhythmic agent with associated hypotensive effects, as well as its additional related potential in myocardial ischemia and related sequellae, and the specific cellular actions that may be responsible for these potential therapeutic effects. Although these include specific actions on both sodium and calcium entry, the focus is on the relevance of independent effects on calcium release. KT-362 relaxes arterial smooth muscle, concomitantly reducing the total peripheral resistance and mean arterial blood pressure. Vascular relaxing actions are attributed primarily to inhibitory effects on calcium release and secondarily to inhibitory effects on calcium entry via both potential-gated and receptor-linked channels. The "intracellular calcium antagonist" properties are correlated with a decrease in the production of the major second messenger, inositol 1,4,5-trisphosphate, which is responsible for calcium release and a concurrent ryanodine-like action that further decreases the amount of calcium released. Ventricular arrhythmias associated with coronary occlusion, cardiac glycosides, catecholamines, and chloroform are prevented by KT-362. General antiarrhythmic properties are associated with a use-dependent block of the "fast" sodium channel, primarily in the activated state, with ancillary effects on the "slow" calcium current. More selective effects on arrhythmias specifically associated with delayed after-depolarizations are attributed to effects on calcium release. In myocardial ischemia, KT-362 primarily reduces myocardial oxygen consumption rather than increases oxygen supply. The former is accomplished by depressing myocardial contractility and reducing afterload, while the latter is associated with a limited effect on coronary collateral blood flow. The negative inotropic effect is fundamentally related to its effects on calcium release, with additional contributions from its effects on calcium entry. Thus, the one intrinsic property of KT-362 that consistently emerges as significant and relevant in cardiovascular disease is the capacity to diminish calcium release.
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PMID:KT-362 related effects on intracellular calcium release and associated clinical potential: arrhythmias, myocardial ischemia, and hypertension. 227 70

The incidence of serum antibodies to human low-density lipoprotein, to oxidized low-density lipoprotein, and to ceroid extracted from human atheroma was assessed in 100 subjects using an adaptation of the enzyme-linked immunosorbent assay technique. Patients with chronic periaortitis, subclinical chronic periaortitis, and ischemic heart disease, and "elderly control" individuals were compared with young, healthy adults. Provided that precautions were taken to prevent oxidation of the low-density lipoprotein during the assay, antibodies were not found to native human low-density lipoprotein. Antibodies to oxidized low-density lipoprotein or ceroid, usually both, were detected in all 20 patients with clinical chronic periaortitis, in 17 of 20 patients with subclinical chronic periaortitis, in 12 of 20 patients with ischemic heart disease, and in 10 of 20 elderly control subjects. Binding inhibition studies showed cross-reactions between oxidized low-density lipoprotein and ceroid. Western blotting after sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that in some patients with clinical chronic periaortitis, these antibodies were directed against breakdown products of apolipoprotein B that resulted from oxidation of low-density lipoprotein. Antibodies to oxidized low-density lipoprotein or ceroid were not detected in healthy young adults. These findings show that chronic periaortitis is accompanied by autoallergy to ceroid, which is probably at least partly composed of low-density lipoprotein oxidized within the human atherosclerotic plaque, and that a number of middle-aged and elderly people without chronic periaortitis also have such antibodies.
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PMID:Serum antibodies to oxidized low-density lipoprotein and ceroid in chronic periaortitis. 232 97


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