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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary cultures of rat heart endothelial cells were subjected to simulated conditions of ischemia: hyposia and glucose deprivation for 4 and 24 hr. Cellular injury was evaluated by measuring changes in viability, total protein, cellular morphology, and leakage of cytoplasmic enzymes from the cells into the culture medium. Deprivation of oxygen and glucose for 4 or 24 hr did not lethally injure the cells as noted by no change in cell viability, morphology, and total protein when compared to controls. However, reversible or non-lethal cellular injury was produced as reflected by a significant release of lactate dehydrogenase (LDH) from the cells into the medium after treatment with hypoxia and glucose deprivation for 4 or 24 hr. When the cultures were deprived of glucose, but were oxygenated, cellular injury was not evident after 24 hr. Deprivation of oxygen but not glucose resulted in significant loss of LDH after 4 or 24 hr. When the cultures were allowed to recover after oxygen and glucose deprivation in complete medium containing 1000 mg glucose per 1 and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures.
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PMID:Injury to primary cultures of rat heart endothelial cells by hypoxia and glucose deprivation. 54 Sep 18

Mongrel dogs (23) were subjected to the experimental study characterizing the effect of noncoronary blood flow upon myocardial mitochondrial respiration. Anoxic arrest for 60 minutes was obtained by cross-clamping of the aorta under hypothermic cardiopulmonary bypass, and heart was reperfused for 10 minutes, then heart was excised to obtain the endocardium, epicardium of the left ventricle and ventricular septum for study of mitochondrial function and myocardial blood flow. Myocardial blood flow was measured with carbonized plastic tracer 46Sc during cross-clamping of the aorta. Noncoronary blood flow showed equal distribution in the left ventricle and septum with flow of 0.16 +/- 0.23 ml/ min/100g (endocardium). Mitochondrial respiratory function following 60 minutes of hypothermic anoxic arrest at 20 degrees C recovered to normal level, and also no correlation was demonstrated between noncoronary blood flow during cross-clamping of the aorta and mitochondrial respiratory function. It was concluded that noncoronary blood flow was negligible with respect to the oxygen demand at 20 degrees C of myocardial temperature, and that noncoronary blood flow during cross-clamping of the aorta was not correlated to mitochondrial protection from ischemia.
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PMID:Effect of noncoronary blood flow upon myocardial mitochondrial function during hypothermic anoxic arrest. 54 86

A reduction in myocardial oxygen supply during ischemia, not only leads to reduced aerobic ATP production but does not stimulate glycolytic ATP synthesis. The residual aerobically synthesized ATP comes primarily from continued inefficient (i.e., compared to glucose in terms of moles of ATP produced per mole of O2 consumed) oxidation of fatty acids. This leads to elevated tissue levels of long chain fatty acyl-CoA and fatty acyl-carnitine. Both are potentially cell damaging metabolic intermediates. Restriction of glycolysis is due to inhibition of glyceraldehyde-3-phosphate dehydrogenase by accumulated metabolites, such as H+, lactate and NADH. The reduced production of ATP leads to decreased levels of high energy phosphate stores which in turn may impair myocardial mechanical function.
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PMID:Energy metabolism in the ischemic heart. 55 21

A method is described to determine local oxygen consumption quantitatively in the brain cortex under in vivo conditions. Local oxygen consumption is calculated from the slope of local tissue PO2 decrease during a few seconds of total ischemia of the brain for each second after the stop of circulation. The decrease of tissue PO2 is recorded simultaneously at several measuring sites. To be independent of oxygen chemically bound to hemoglobin, tissue PO2 values are raised above 100 Torr. The calculation of local oxygen consumption for each second during the short period of ischemia showed that the O2 consumption remains constant only for a few seconds ranging from 5 to maximally 15 s at different locations. The O2 consumption decreases continuously although the tissue PO2 values are still above the full saturation of hemoglobin. The rate of local oxygen consumption varies considerably at different measuring sites of the superficial layers of the brain cortex (cat). The mean value amounts to 3 +/- 1.5 ml O2/100 g tissue and minute.
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PMID:Direct determination of local oxygen consumption of the brain cortex in vivo. 56 39

Chronic hypoxemia was produced in 16 dogs by surgical transposition of the caudal vena cava to the left atrium to determine if chronic hypoxemia would alter the response of the myocardium to acute ischemia. An electromagnetic aortic flow probe, left atrial tube, and occlusive cuff on the left circumflex coronary artery were permanently implanted in 11 hypoxemic and 26 normal control dogs. The animals were studied in the conscious state after recovery from the surgery. Dogs with hypoxemia had a blood hematocrit value of 54.3 +/- 1.0% (SE), arterial PO(2) of 43.2 +/- 1.4 mm Hg, and 80.2 +/- 1.6% oxygen saturation. There was no difference from control animals in the ratio of left ventricular weight to body weight, but the right ventricular weight was significantly decreased in the hypoxemic dogs. Cardiac output from the left ventricle was twice that of the right ventricle. Aortic blood flow was 3.68 +/- 0.22 liters/min in hypoxemic animals and 2.64 +/- 0.19 liters/min in normal dogs. Myocardial blood flow measured with 15-mu diameter tracer microspheres was increased from 79 +/- 10 and 59 +/- 8 ml/100 g/min in left ventricular endocardial and epicardial halves, respectively, in normal dogs to 212 +/- 48 and 172 +/- 39 in dogs with chronic hypoxemia. There were no deaths in 10 hypoxemic dogs within 24 hours after complete circumflex coronary artery occlusion; 7 of 26 (27%) normal dogs died after circumflex coronary artery occlusion during the conscious state. Gross infarct size was extremely variable in both groups. Median infarct size was smaller in dogs with hypoxemia and was directly correlated with arterial PO(2) in hypoxemic dogs. There was a mild, but statistically not significant, increase in the anastomotic index of hypoxemic dogs compared with that of normal animals, suggesting that a metabolic adaptive change rather than increased collateral circulation may have been responsible for the decreased mortality and smaller infarct size in hypoxemic dogs.
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PMID:The effect of chronic hypoxemia on regional myocardial blood flow in the conscious dog after acute coronary artery occlusion. 59 17

The effect of KoQ4 on the energetics, contractility, and electrogram of the ischemized myocardium was studied in acute experiments on dogs with induced myocardial ischemia. Intracornoary administration of KoQ4, 1.3 mg/kg, directly into the focus of ischemia for 15 min promoted a decrease in the lactate level in blood draining from the ischemic zone as compared to the control data in the absence of a difference in the dynamics of the pyruvic acid content. In distinction to the control experimental series, there was no decrease in the concentration of glucose in samples of venous blood draining from the focus of ischemia. Under the effect of KoQ4 the amplitude of left ventricular pressure and the maximum rate of its growth (dp/dt) increased moderately and the ST segment and ST/R coefficient of the epicardial electrogram from the border zone of ischemia decreased. It was shown in the rat experiments that preliminary intravenous administration of KoQ4 (14 mg/kg) increased myocardial resistance to oxygen deficiency under conditions of diacetylcholine-induced apnoe.
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PMID:[Effect of hexahydroubiquinone-4 (KoQ4) on the bioenergetics and functional activity of the myocardium in ischemia]. 59 31

A model to study pressure-induced ischemia by intravital microscopy is presented. A hamster cheek pouch is prepared to get a single layer of epithelium, together with vessels and connective tissue. Pressure, which can be varied, is transmitted to the tissue by a pressure chamber with a rubber membrane. Microcirculatory reactions may be studied while the pressure is applied, when the pressure is released and as the tissue is regaining circulation. The local environment is controlled by irrigating the test tissue with a solution approximating the composition of interstitial fluid. Local oxygen and carbon dioxide tensions are controlled. There is a marked difference in restoration of blood flow to the tissue after 2- and 4-hour ischemia. After 2-hour ischemia the tissue regained circulation rapidly. Microbleedings developed during the postpressure observation time. After 4-hour ischemia, on the other hand, the tissue regained circulation slowly and only in one third of the microvessels. Extensive white blood cells sticking to the vessel walls were seen indicating endothelial damage. In the 4-hour experiments there were very few microbleedings compared to the 2-hour experiments.
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PMID:Pressure-induced ischemia. I. An experimental model for intravital microscopic studies in hamster cheek pouch. 60 63

Twenty-seven patients undergoing open-heart surgery were divided into three groups, i.e., control, intermittent aortic crossclamping and coronary perfusion groups. Myocardial oxygen extraction, lactate extraction, arterial-coronary sinus hydrogen ion difference, potassium difference and glucose difference were determined during the operation, as well as, postoperative stroke and cardiac indices and comparisons were made. When the ascending aorta was not crossclamped, myocardial metabolism was well preserved during and after the perfusion at a flow rate of 2.0 L./min/m2. Intermittent aortic crossclamping for 15 minutes alternating with a period of perfusion for five minutes at 30 degrees C was sufficient to protect the myocardium from ischemia. Perfusion of the left coronary artery alone at a flow rate of six per cent of total body perfusion (150 to 200 ml per minute) at 30 degrees C was sufficient to protect the myocardium when the aorta was opened. Since intermittent perfusion of the left coronary artery may produce myocardial derangement, coronary perfusion should be continuous. Otherwise topical cardiac cooling or other means of myocardial protection should be used.
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PMID:Myocardial protection during open-heart surgery: intermittent aortic crossclamping versus coronary perfusion. 60 90

The effect of pulsatile cardiopulmonary bypass on intramyocardial gas tensions and regional myocardial blood flow was studied in 10 mongrel dogs. Following application of a critical stenosis to the circumflex coronary artery (CIRC), animals were placed on total bypass with vented, fibrillating hearts. During three 45 minute periods of perfusion, animals alternately received pulsatile or linear flow with perfusion pressure carefully maintained at 80 mm. Hg. In myocardium supplied by the stenosed CIRC, intramyocardial oxygen tension (PO2) rose from 13 +/- 3 to 19 +/- 5 mm. Hg when a period of linear flow was followed by a period of pulsatile flow (p less than 0.025). Similarly in the CIRC-supplied area, intramyocardial carbon dioxide (PCO2) decreased from 128 +/- 12 to 99 +/- 12 mm. Hg (p less than 0.005) with conversion from linear to pulsatile flow. Myocardial blood flow (microsphere technique) to endocardial and epicardial layers of the CIRC-supplied area was significantly greater (p less than 0.05) during pulsatile than during linear perfusion. In contrast, when periods of pulsatile bypass were followed by periods of linear perfusion, myocardial PO2 fell from 25 +/- 6 to 9 +/- 3 (less than 0.02) and myocardial PCO2 rose from 82 +/- 12 to 154 +/- 12 mm. Hg (p less than 0.001). These data suggest that (1) fibrillation-induced regional ischemia distal to a critical coronary stenosis can be reduced by pulsatile perfusion during bypass and (2) the mechanism for the reduction in regional ischemia is improved myocardial blood flow.
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PMID:Comparison of regional myocardial blood flow and metabolism distal to a critical coronary stenosis in the fibrillating heart during alternate periods of pulsatile and nonpulsatile perfusion. 62 24

Myocardial ischemia at rest occurs only late in the course of coronary artery disease, but transient ischemia can often be induced by increasing myocardial oxygen demand with exercise or atrial pacing. Myocardial ischemia causes a series of physiologic abnormalities that can be detected by assessment of myocardial perfusion, regional mechanical function, electrophysiology, and metabolism. Methods of assessment vary widely in sensitivity, specificity, cost, and ease of application. Although the appropriate choice of diagnostic test may be difficult, the morbidity and mortality that result from myocardial ischemia and infarction and the demonstrated potential of coronary artery bypass surgery to reverse myocardial ischemia before the development of permanent sequellae make the detection of ischemia an important clinical problem. Present methods for quantitating myocardial ischemia are imprecise and difficult to apply but have been used successfully to evaluate the efficacy of therapies designed to reduce the size of myocardial infarction.
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PMID:Myocardial ischemia: detection and quantitation. 62 55


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