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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

We measured the extravascular water content of hearts and lungs of anesthetized dogs subjected to one of the following protocols: a)sham operation, b) circumflex artery ligation, c) increased left atrial pressure (Pla), or d) increased Pla and circumflex artery ligation. After 4 h, extravascular water of the heart and lungs increased significantly in the three experimental groups when compared with values from sham-operated dogs. After circumflex artery ligation, extravascular heart water increased 29% and lung water 8%, although Pla and calculated pulmonary microvascular pressure (Pmv) did not change. Extravascular heart water also rose 30% after increasing Pla from 23 to 37 cm H2O by inflating a left atrial baloon. In these dogs, extravascular lung water increased as a hyperbolic function of Pmv. Increasing Pla to 20 cm H2O in dogs with coronary artery ligation resulted in a 16% increase in heart water. Also at each Pmv, extravascular lung water was greater in dogs with coronary artery ligation than in dogs without. These data indicate that the increased extravascular lung water after coronary artery ligation cannot be explained solely by hemodynamic mechansims. We suggest that acute myocardial ischemia contributes to an increase in vascular permeability in the heart and lungs.
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PMID:Extravascular water content of heart and lungs after acute myocardial ischemia. 67 21

Repeatedly bred male rats which develop arteriosclerosis spontaneously were subjected to unilateral nephrectomy, 1% saline drinking water, and 2 mg subcutaneous injections of deoxycorticosterone acetate per animal weekly for 7 weeks to induce severe hypertension (+/- 175 mmHg systolic). Acute cerebral ischemia was induced by ligating one carotid artery. Two days later, experimental animals were subjected to acute myocardial ischemia by injecting them subcutaneously with a single dose of isoproterenol (25 mg/100 g body weight). All of the experimental animals died within 4 hours of the injection of isoproterenol. During this same period, blood pressure, body weight, thymus, kidney, and testicular weights were reduced, whereas heart and adrenal gland weights increased markedly. Serum enzymes (CPK, SGOT, and LDH), lipids (triglycerides and free fatty acids), glucose, BUN, and corticosterone rose progressively. Fatty infiltration of the liver, adrenal hyperplasia, myocardial thrombi, renal degenerative changes, and cerebral edema became progressively more severe. A hypothalamic-pituitary-adrenal axis component may be involved in the reaction to the stress of acute cerebral or myocardial ischemia, which is intensified when the two ischemias are combined, and chronic hypertension may exacerbate both.
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PMID:Acute cerebrovascular and myocardial ischemia superimposed upon chronically hypertensive and arteriosclerotic male Sprague-Dawley rats. 90 14

Reperfusion following myocardial ischemia has been postulated to cause myocardial edema resulting in increasing interstitial pressure and retardation of the microcirculation. If ischemia then is repeated, the additional insult results in increasing edema and possible infarction. In order to test this hypothesis, 15 pigs were placed on cardiopulmonary bypass with coronary perfusion maintained at 100 mm. Hg by a separate pump through the clamped aortic root. Coronary flow and vascular resistance were recorded. Distribution of coronary blood flow was monitored by injection of radioactively labeled microspheres (15 mu). Myocardial extravascular water was measured by simultaneously determining myocardial intravascular water with radioactive iodinated serum albumin (RISA) and total myocardial water with tritiated water (THO). Three 30 minute periods of myocardial ischemia and 5 minutes of coronary perfusion produced (1) a loss of the reactive hyperemic response to ischemia (coronary vascular resistance increased--from 0.295 +/- 0.024, control, to 0.366 +/- 0.042, after anoxia--rather than decreasing with reactive hyperemia induced vasodilatation); (2) a significant maldistribution of coronary flow away from the endocardium (endocardial: epicardial perfusion ratio 1.10 +/- 0.05, control, to 0.69 +/- 0.08, following ischemia, p less than 0.05); and (3) significant myocardial edema. Myocardial extravascular water rose from 46.4 +/- 1.7 ml. per 100 Gm., control, to 52.6 +/- 2.0 ml. per 100 Gm., after ischemia (p less than 0.05), whereas intravascular myocardial volume did not change significantly. Both light and electron microscopic examination of the postischemic myocardium shows interstitial and intracellular edema with typical ischemic changes at a cellular and subcellular level. The significant increase in myocardial extravascular water content associated with this injury supports the concept that myocardial reperfusion plays a role in its development.
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PMID:Myocardial reperfusion, a cause of ischemic injury during cardiopulmonary bypass. 94 Oct 98

The state of the water-electrolyte metabolism was studied by the radio-isotope dilution technique in 115 patients with different forms of ischaemic heart disease and in 25 normal persons. It was established that all forms of ischaemic heart disease are accompanied by a significant potassium deficit imperceptible for blood and urine examinations of their electrolyte composition. The potassium deficit is most clearly expressed in patients with cardiosclerosis, especially in congestive heart failure. In a considerable part of the patients with acute myocardial infarction, including those without clinical signs of congestive heart failure, the rate of sodium and water metabolism is decreased, and the total body content of metabolizing sodium is increased. Sodium retention in the body is especially severe in patients with cardiosclerosis complicated by congestive circulatory insufficiency. The administration of diuretics in adequate doses was shown to result in normalization of the indices of sodium and water metabolism.
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PMID:[State of water-electrolyte metabolism in ischemic heart disease]. 101 7

Twenty normal subjects and 32 patients with ischemic heart disease (IHD) were subjected to submaximal treadmill exercise. The mean transthoracic electrical impedance (TEI) was measured with a tetrapolar lead system and the changes were correlated to the extent of ST depression observed on an on-line digital computer. Six subjects of pre-excitation syndrome with "false" ST depression were also studied. The normal subjects did not show a significant change of TEI during exercise. The patients with IHD showed a steady and significant decrease in TEI, correlating with the extent of ST depression. Recovery was slow after the cessation of exercise. The subjects with false ST changes showed no decrease of TEI. The changes were more profound in subjects who developed anginal pain during the test. These findings are attributed to an increase in the thoracic blood volume and pulmonary extravascular water due to transient left ventricular dysfunction in angina.
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PMID:Changes in transthoracic electrical impedance during submaximal treadmill exercise in patients with ischemic heart disease--A preliminary report. 110 66

A comparison is made between mortality from ischaemic heart disease and the quality of drinking water in the cities of Brisbane and Melbourne. Mortality from ischaemic heart disease is found to be higher in Brisbane where drinking water is harder, than in Melbourne. Moreover, mortality from all causes is higher in Brisbane than in Melbourne.
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PMID:Ischaemic heart disease and the water factor. A variable relationship. 118 59

1. There is no known cause for the increased mortality due to ischaemic heart disease in soft water areas. Since the lead concentration of soft water is elevated in houses with lead plumbing, studies have been carried out to determine the effects of lead on the heart of rats. 2. Rats were given drinking water containing lead for 1 year at concentrations similar to those found previously in Glasgow, which has a soft water supply. 3. There was increasing deposition of lead in the heart and a fall in the cardiac levels of the enzymes ferrochelatase and delta-aminolaevulinic acid dehydratase. These changes are maximal after 6 months, when there were marked electron-microscopic changes in the myocardium and myocardial mitochondria. 4. Further studies are needed to determine whether lead is a cause of the increased mortality from ischaemic heart disease in soft water areas.
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PMID:Cardiac effects of lead in drinking water of rats. 119 93

Rabbit hearts were perfused at a pressure of 60 cm H2O with 37 degrees C Tyrode solution aerated with 5% CO2 in O2. The effluent from the heart was collected in four consecutive 10-min periods. The samples were analyzed for prostaglandins of the E series (PGE), using thin layer chromatography for identification and assay on the superfused rat stomach strip for quantitative estimation. Three different series of experiments were performed, the hearts in each series during the second effluent collection period being perfused under conditions of either hypoxia (Tyrode solution aerated with 5% O2 and 5% CO2 in N2), absence of glucose in the Tyrode solution, or hypotension/low perfusion flow (perfusion pressure lowered to 30cm H2O). In the series where glucose was omitted or hypotension/low perfusion flow was induced during the second effluent collection period, the outflow of PGE decreased exponentially throughout the four periods. In the series where hypoxia was maintained during the second effluent collection period, a marked increase in the outflow of PGE was noted after the end of hypoxia. Prostaglandins of the E series are powerful vasodilators, and the PG released may, by inducing coronary vasodilation, counteract the hypoxia. However, it has been shown that, in human plasma, conversion of arachidonic acid to PGE is parallelled by platelet aggregation. Therefore, if PG synthesis is also stimulated by hypoxia in man, myocardial ischemia must be considered as a possible mechanism for platelet aggregation and subsequent coronary thrombosis.
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PMID:Hypoxia-induced prostaglandin release from rabbit heart. 120 90


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