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

The nephrotic syndrome is the only hypoalbuminaemic state frequently associated with hyperlipidaemia. In the presence of a negative nitrogen balance, hyperlipidaemia is metabolically inappropriate and reflects the result of persistent breakaway from free fatty acid control. This lipid abnormality may result in the premature development of ischaemic heart disease in patients in whom it is not possible to control the primary renal abnormality. The authors suggest that future work should be directed towards thyroxine and insulin metabolism in nephrotic states.
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PMID:Biochemical anomalies of the nephrotic syndrome. 16 35

Ibuprofen, a nonsteriodal anti-inflammatory agent, was studied in the early stages of myocardial ischemia in order to determine whether it helps preserve myocardial integrity. Ibuprofen was administered intravenously at a dose of 12.5 mg/kg at the time of coronary artery occlusion and again 2.5 h later. Ibuprofen significantly prevented the loss of myocardial creatine phosphokinase (CPK) release in ischemic cardiac tissue. In addition, this drug significantly returned S-T segment elevation toward normal values, and significantly prevented the myocardial loss of compounds having free amino nitrogen groups, an index of proteolysis. Although ibuprofen moderated the increased plasma CPK activity, plasma CPK values 5 h after coronary occlusion were above control values. Thus, ibuprofen significantly prevented alterations in three of the four indices used to assess myocardial ischemic damage. The protective mechanism of ibuprofen may be via stabilization of cellular membranes (i.e., lysosomal membranes) and to a lesser extent on reduction in myocardial oxygen demand.
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PMID:Beneficial effects of ibuprofen in acute myocardial ischemia. 47 33

Verapamil, at a dose of 1 mg/kg, was given intravenously to anesthetized cats one hour after coronary artery occlusion. Verapamil significantly reduced mean arterial blood pressure, but produced an increase in heart rate, partially offsetting the reduction in myocardial oxygen demand resulting from the reduction in pressure. Verapamil failed to prevent the elevations in the S-T segment of the electrocardiogram observed in cats subjected to myocardial ischemia (MI) and given only the vehicle for verapamil (i.e., 0.9% NaCl). Moreover, verapamil also did not prevent the accumulation of creatine phosphokinase (CPK) activity in the circulating blood after MI. Nevertheless, verapamil significantly prevented the loss in CPK and in amino-nitrogen observed in the ischemic region of the myocardium, indicating some protective effect on myocardial integrity. The major effects of verapamil on electrolyte content of ischemic myocardial tissue were a decrease in sodium and an increase in potassium. However, calcium gain by the heart was not prevented by verapamil. Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.
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PMID:Influence of verapamil on cellular integrity and electrolyte concentrations of ischemic myocardial tissue in the cat. 52 60

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.
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PMID:Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs. 59 70

The effect of induced myocardial ischemia on cardiac glycogen utilization was investigated in trained and untrained male Sprague-Dawley rats. Following a 12 to 15 week endurance training program, myocardial ischemia was induced by ligation of the left coronary artery. Prior to and at 5 min intervals following ligation, affected tissues of five trained and untrained animals were removed, frozen in liquid nitrogen, and analyzed for glycogen and lactic acid. The glycogen content for both groups declined significantly (p less than 0.05) during the first 5 min, 38% and 15% for the trained and untrained, respectively, with a concomitant rise in the lactic acid of 150% and 40%. Overall, the cardiac lactate in the trained hearts was lower (p less than 0.05) than in untrained hearts but the pattern of response was the same. During the final 5 min of ischemia, cardiac glycogen rose in the trained hearts and declined in the sedentary hearts. The difference between the two groups at 30 min was significant (p less than 0.05). The results show that trained and untrained rat hearts utilize glycogen differently but produce similar quantities of lactic acid during brief periods of myocardial ischemia. Similar lactate despite greater glycogen utilization may indicate reduced anaerobic stress in the trained rat heart.
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PMID:Cardiac glycogenolysis in trained and untrained ischemic rat hearts. 179 20

Calcium channel antagonists are commonly used to treat chronic hypertension. Several studies of intact vascular tissues suggest that these agents may impair the production of the endothelium-derived relaxing factor and alter endothelium-dependent vascular relaxation. These studies are difficult to interpret because the calcium channel antagonist may have direct effects on vascular smooth muscle. In our study, a chemiluminescence assay was used to measure the release of nitrogen oxides from bovine aortic endothelial cells (BAEC) grown in monolayer. Under basal conditions, the release of nitrogen oxides was 0.2 nmol/100 mg protein and was increased approximately two-fold by 0.1 micrograms, bradykinin. Incubations with diltiazem, verapamil, and nifedipine for 60 min did not influence the basal and bradykinin-stimulated release of nitrogen oxides by BAEC. These data illustrate that the production of the endothelium-derived relaxing factor is not altered by the calcium channel antagonist, and are compatible with an absence of L-type calcium channels in vascular endothelial cells. Chronic hypertension produces myriad adverse effects in the coronary circulation. After coronary occlusion, infarct size, expressed as a function of myocardial mass perfused, is increased by 33%, and the wavefront of infarction from subendocardium to subepicardium is hastened. Both chronic and acute hypertension produce numerous abnormalities of coronary flow regulation. These include impairments of autoregulation, changes in vascular responsiveness, and alterations of endothelial cell function. Many of these may worsen the clinical consequences of ischemic heart disease, either by producing structural alterations of the coronary vasculature, or equally importantly, by altering coronary vascular responsiveness to either mechanical or neurohumoral stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and the coronary circulation. With special attention to endothelial regulation. 191 Jun 38

This study was designed to test the usefulness of nitrogen-13 (N-13) glutamate imaging with positron emission tomography in defining myocardial ischemia in humans. Seventeen patients who had undergone coronary arteriography were studied with N-13 glutamate at peak supine exercise using a bicycle ergometer, as well as with the flow tracer N-13 ammonia at peak exercise during a second similar exercise test. Six of the patients also underwent imaging with N-13 glutamate at rest before exercise testing; in the remaining 11 patients imaging with fluorine-18 (F-18) fluorodeoxyglucose was performed to assess glucose metabolism after the second exercise test. Seven patients had classic metabolism-flow mismatches consistent with ischemia (that is, decreased N-13 ammonia uptake in a region with relatively increased F-18 fluorodeoxyglucose uptake). There was no evidence of increased N-13 glutamate uptake in the ischemic mismatched regions in any of these patients. In all 17 patients, the uptake of N-13 glutamate during exercise paralleled the uptake of N-13 ammonia during exercise, suggesting that N-13 glutamate behaves as a flow tracer rather than as a metabolic marker of ischemia in humans.
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PMID:Dynamic positron tomographic imaging with nitrogen-13 glutamate in patients with coronary artery disease: comparison with nitrogen-13 ammonia and fluorine-18 fluorodeoxyglucose imaging. 197 78

The low-energy protein diet providing 1559 kJ is the first accurately defined diet for the treatment of obesity in the CSSR. The daily amount contains 4.0 g fat, 33.0 g protein, 50.0 g carbohydrate, 5.6 g fibre and daily recommended allowances of vitamins. The diet is enriched with potassium, magnesium and iron. The low-energy protein diet was used for a period of 28 days in the treatment of 49 obese patients aged 40.49 +/- 1.39 years whose initial weight was 110.14 +/- 3.41 kg and the BMI 39.44 +/- 1.13. The therapeutic regime comprised in addition to the diet adequate physical exercise of aerobic character and training of correct eating behaviour. Four weeks treatment led to a significant decline of body weight (by 10.60 +/- 0.46 kg) and a significant drop of the BMI (by 3.65 +/- 0.16). Men lost more weight than women. In women a substantial drop of the body weight (90.5%) was due to reduction of body fat, while in men adipose tissue participated by 60.0% in the loss. During the fourth week of treatment a positive nitrogen balance was achieved, obviously due to adequate physical exercise. The waist/hip ratio was not affected by treatment in either group. The therapeutic regime influenced favourably some risk factors of ischaemic heart disease. In addition to a significant drop of the systolic and diastolic blood pressure a significant decline of total cholesterol, triacylglycerols and serum insulin occurred. There was a concurrent decline of the urinary C-peptide excretion. The therapeutic regime involving the low-energy protein diet was well tolerated by the patients. The incidence of side effects during treatment was less frequent than in treatment by intermittent fasts. No disorders of the cardiac rhythm were recorded during treatment.
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PMID:[A Czechoslovak low-energy protein diet in the treatment of obesity]. 235 13

Cardiovascular, platelet- and neutrophil-inhibitory effects of the chemically stable prostacyclin analog nileprost (5-cyano-16-methyl-PGI2) (NIL, ZK 34798) were studied in vitro and in a feline model of acute myocardial ischemia in vivo. Isolated bovine coronary arteries were relaxed by NIL at low concentrations (less than 3 microM), whereas higher concentrations produced a marked vasoconstriction. NIL inhibited human platelet aggregation and reduced the coronary vascular resistance of Langendorff-perfused rabbit hearts. Myocardial contractile force and oxygen consumption were not affected. The superoxide anion generation of stimulated granulocytes was modestly antagonized by NIL. NIL (0.5 microgram/kg/min intravenously, i.v.) protected the left ventricular myocardium of cats subjected to 5 h of coronary artery ligation from ischemic injury, as evidenced by the reduction in ischemia-induced ST-segment elevation, prevention of the large increase in plasma creatinine kinase (CK), and loss of myocardial CK and free amino nitrogen. These effects and the extent of cardiac protection by NIL were comparable to those of PGI2 (0.2 microgram/kg/min), whereas PGE2 (1.5 microgram/kg/min) was less effective. The data demonstrate a combination of PGI2-like and PGE2-like activities for NIL in vitro and a significant cardioprotective action of NIL in vivo.
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PMID:Cardiovascular actions in vitro and cardioprotective effects in vivo of nileprost, a mixed type PGI2/PGE2 agonist. 244 Nov 64

There is a growing evidence for the role of oxygen free radicals (OFR) in mediating myocardial tissue injury during myocardial ischemia and particularly during reperfusion. But almost all of the evidence was indirect, using electron spin resonance (ESR) spectroscopy, we have directly measured OFR generated in ischemic and reperfused isolated rabbit hearts. 17 hearts were rapidly frozen in liquid nitrogen after their arrest by cardioplegic solution and sampled after 150 min of sustained hypothermic global ischemia or after reperfusion. The ESR spectra obtained from experiment have directly demonstrated that OFR is produced in significant amounts in the isolated rabbit hearts during early stage of reperfusion but only small amount during ischemia. The mitochondrial electron transport chain appeared to be the main source of OFR. We found that superoxide dismutase scavenged OFR generated during reperfusion efficiently, but catalase did not. We believe that superoxide anion, not hydroxyl radical, is the main OFR which is responsible for myocardial reperfusion injury. We also found that Salvia, a traditional Chinese medicine, a very efficient OFR scavenger, had the similar effect as superoxide dismutase.
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PMID:[Direct detection of oxygen free radicals produced by myocardial reperfusion using electron spin resonance spectroscopy]. 255 94


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