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)

An in vitro model of myocardial ischemia has been established with primary monolayer cultures of postnatal rat myocardial cells. Ischemic conditions were simulated in vitro by subjecting the myocardial cell cultures to various levels of oxygen and glucose deprivation. The experimental protocol consisted of treatment with 20% or 0% O2 and 1000, 500 or 0 mg glucose per 1 of medium for 4 or 24 hr. Control cultures were treated with 20% O2 and 1000 mg glucose. After the ischemic treatments, cultures of beating muscle (M) cells were evaluated for signs of injury, i.e. leakage of cytoplasmic enzymes into the culture medium. Differences were found in leakage of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) from the cultures that were exposed to partial ischemia of glucose deprivation and from those cultures that were exposed to total ischemia of oxygen and glucose deprivation. Glucose deprivation along resulted in a slight-to-moderate loss of LDH and CPK from the cells, whereas total ischemia resulted in a significant release of the two cytoplasmic enzymes. When the cultures were allowed to recover after ischemic treatment in complete medium (1000 mg glucose) and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures. Cell viability and total protein content of the ischemic cultures did not differ significantly from controls.
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PMID:Ischemic myocardial injury in cultured heart cells: leakage of cytoplasmic enzymes from injured cells. 68 9

One hundred sixteen patients with suspected or proven coronary arterial disease underwent rapid atrial pacing until the occurrence of pain in the chest or a heart rate of at least 160 beats per minute. Significant elevation of arterial systolic pressure of 25 percent or more above control was observed in 17 patients. Each of these patients had significant coronary arterial disease shown by coronary arteriographic studies. During rapid atrial pacing, each of these 17 patients had pain in the chest and ST-segment changes suggesting ischemia, and 15 had abnormal (less than 10 percent) extraction of myocardial lactate. In the 99 patients who did not have increased arterial systolic pressure during rapid atrial pacing, the frequencies of coronary arterial disease, ischemic ST-segment changes, and abnormal extraction of lactate during rapid atrial pacing were significantly (P less than 0.05) less. Increased arterial systolic pressure during rapid atrial pacing appears to be highly indicative of coronary arterial disease and myocardial ischemia. We suggest that myocardial ischemia may, under certain circumstances, be responsible for short-term increases in arterial pressure.
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PMID:The role of myocardial ischemia in pacing-induced elevation of arterial pressure. 69 47

25 anesthetized mongrel dogs underwent a left thoracotomy. Creatine kinase (CK) activity was measured in serial blood samples drawn simultaneously from the aorta and a coronary vein. The distribution of myocardial perfusion was determined by a continuous infusion of krypton-81m (half-life 13 sec) into the aortic sinuses. Heart rate and arterial blood pressure were also measured throughout the procedure. In 20 dogs regional myocardial ischemia was produced by ligation of a major branch of the left anterior descending coronary artery. Five of these dogs received 1 microgram.kg-1 nifedipine i.v. and a further 5 received 13 microgram.kg-1. Thoracotomy alone produced a slight rise in plasma CK activity but the arteriovenous difference (AV) across the segment of the heart remained positive over 5 h. Myocardial ischemia in the untreated dogs caused a considerable increase in CK activity and the AV difference became negative at 90 min. Treatment with the lower dose of nifedipine considerably reduced the plasma CK activity and the AV difference did not become negative until 3 h. Regional myocardial perfusion showed a significant improvement. Conversely, the higher dose of nifedipine produced a marked increase in the area of ischemia and an acceleration of CK release from the heart. This was associated with a decrease in arterial pressure and an increase in heart rate. These results show that nifedipine can be beneficial in experimental myocardial infarction but care must be taken to avoid hypotension and increases in heart rate.
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PMID:Effects of nifedipine on creatine kinase release during myocardial ischemia in dogs. 69 37

Epicardial ECG signs have been studied in 26 anesthetized and thoracotomized dogs in an attempt to follow the progress of tissue damage during regional myocardial ischemia. Epicardial ECG's were recorded before and during 15 min, 1 and 5 h of severe left anterior descending coronary artery narrowing. Epicardial ST segment elevation followed a complicated natural history. An analysis of variance showed the significant effects of respiration, heart rate and changes in time during myocardial ischemia. Regional epicardial R waves showed a transient increase in amplitude following coronary narrowing. There was no loss of electrically active myocardium following 15 min of ischemia. Irreversible loss of R waves were noted at between 30 and 45 min and progressed to full development within 5 h following coronary artery narrowing. The loss of electrically active myocardium (R loss plus Q waves) at 5 h was closely related to the myocardial depletion of creatine kinase activity (mu/mg DNA-1) at 24 h in each dog. The early manifestation of myocardial ischemia (ST segment elevation at 17 min) was closely related in the later evidence of cell death (R loss plus Q waves) in each dog. These relationships were less precise when the results were combined and this showed the variability between dogs in heart size and infarct size. The study suggested that the individual complete natural history of these ECG signs must be studied before they can be used to assess the extent and progress of myocardial ischemia and cell death.
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PMID:Electrocardiographic signs in experimental myocardial ischemia and infarction. 69 50

We studied the role of cardiopulmonary vagal afferents in the cardiovascular responses to coronary artery occlusion in conscious dogs with intact carotid sinuses and following functional denervation of the arterial baroreceptors. The contributions of vagal afferents were determined by cold blocking the vagi. In dogs with intact carotid sinuses, coronary artery occlusion produced small decreases in mean cardiac output and arterial pressure, whereas heart rate increased by 35 beats/min. In dogs with intact carotid sinuses, vagal cold block increased mean arterial pressure by 22 +/- 2 (mean +/- SE) mm Hg and heart rate by 90 +/- 6 beats/min. Mean cardiac output increased by 505 +/- 90 ml/min. With the exception of heart rate, responses to coronary occlusion during vagal cold block were similar to the occlusion response prior to vagal cold block. Furthermore, prior occlusion of the coronary artery did not significantly influence the responses to vagal cold block. After arterial baroreceptor denervation, coronary artery occlusion resulted in a substantially greater fall in systemic arterial pressure (-52 mm Hg as compared to -8 mm Hg, with intact carotid sinuses) and peripheral resistance decreased by -0.49 peripheral resistance units (PRU). Vagal cold block following denervation increased the arterial pressure by 49 +/- 10 mm Hg and peripheral resistance by 0.59 +/- 0.13 PRU. Both values were significantly greater than those observed during vagal cold block prior to denervation. In arterial baroreceptor-denervated dogs, vagal blockade significantly attenuated the response to coronary occlusion. Therefore, in conscious dogs, vagal afferents from cardiopulmonary receptors exert a significant inhibitory influence on the peripheral vascular tone. When the carotid sinuses are intact, this inhibitory influence appears to be marked during myocardial ischemia. In the absence of functional arterial baroreflexes, vagal afferent activity contributes to the depressor responses observed during ischemia.
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PMID:The circulatory influences of vagal afferents at rest and during coronary occlusion in conscious dogs. 70 45

It is not known whether ventricular relaxation can be altered by ischemia independent of associated hemodynamic changes. The effect of acute myocardial ischemia on diastolic relaxation was studied under controlled hemodynamic conditions in 16 anesthetized dogs on right-heart bypass. In nine dogs, left ventricular end-diastolic pressure was maintained constant throughout the experiments. Ischemia produced a significant prolongation of the isovolumetric relaxation period (IVRP) from 29 +/- 3 (SE) to 88 +/- 7 ms (P less than 0.01). Ischemia, per se, the associated decrease in contractility, or the fall in peak left ventricular pressure (LVP) may have contributed to the increase in IVRP. The latter was not the only mechanism involved, because in seven dogs studied with constant peak LVP, IVRP again was prolonged from 64 +/- 8 to 95 +/- 8 ms (P less than 0.01). Moreover, in five nonischemic hearts in which peak LVP was maintained constant, contractility was decreased by sodium pentobarbital to the same extent as with ischemia; IVRP did not change. Thus, the additional prolongation of the IVRP in the ischemia experiments is secondary to a direct effect of ischemia on the relaxation process of the myocardium.
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PMID:Effects of acute global ischemia on diastolic relaxation in canine hearts. 73 60

The effects of 30-, 60-, and 90-min occlusion of the left anterior descending coronary artery and 60-min reperfusion were studied on the left ventricular dP/dt, myocardial ultrastructure, and tissue as well as blood lactate levels in dogs. The dP/dt was depressed by the occlusion, and reperfusion instituted after 30 min resulted in full recovery whereas that after 90 min had an adverse effect. Varying degrees of ultrastructural damage were noted after 60 and 90 min of occlusion and this was further exaggerated by reperfusion. Coronary occlusion markedly increased lactate content of ischemic myocardium, and the same returned to normal upon reperfusion. Myocardial ischemia for 30 or 60 min did not affect net arterial lactate extraction by the heart, but ischemia for 90 min reversed net lactate extraction to net lactate production by the heart. Reperfusion after 30 min of occlusion significantly increased lactate extraction, but reperfusion after 60 and 90 min of ischemia significantly decreased net lactate extraction and increased net production, respectively. The results indicate that estimation of net lactate exchange across the heart can be of value in assessing the viability of myocardium following coronary bypass surgery.
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PMID:Arterio-venous difference in lactate levels in myocardial ischemia and reperfusion. 74 23

To determine whether vagal activity during myocardial ischemia functions to stabilize the heart, the left anterior descending coronary artery in dogs was occluded for periods of 3 1/2 minutes with and without concurrent vagal stimulation. Bipolar electrograms were measured from the surface of the canine left ventricle within and outside the regions of intended ischemia. Ischemia in the absence of vagal stimulation depressed both the electrogram amplitude and the upstroke velocity of the electrogram signal. Vagal stimulation significantly decreased the absolute magnitude of the ischemia-induced decrease of the electrogram signal, which indicates that it tended to stabilize the insulted heart. This stabilizing influence however, was seen only in the presence of adrenergic blockade with practolol. The vagal response was only partially blocked by atropine, whereas it was abolished by lidocaine. These results suggest that a vagally mediated stabilization of the ischemic canine ventricle can occur and is unmasked only in the absence of sympathetic neural activity.
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PMID:Vagal stabilization of the ischemic canine ventricle. 75 31

We studied 25 anesthetized and thoracotamized dogs before and during 5 hours of acute regional myocardial ischemia. Krypton-81m (81mKr) was infused constantly into the aortic sinuses. The myocardial equilibrium of this tracer was used to image and assess the distribution of regional myocardial perfusion using a gamma camera and digital computer. The epicardial ECG was recorded, S-T segment elevation and the loss of R and appearance of Q waves were measured, and the plasma activity of creatine kinase (CK) was determined in aortic and coronary venous blood throughout these experiments. Ten dogs underwent left anterior descending coronary artery (LAD) narrowing for 5 hours and received no drugs. Five dogs received nifedipine 13 microgram/kg, and another five received 1.0 microgram/kg intravenously 30 minutes after LAD narrowing. Those dogs receiving nifedipine, 13 microgram/kg, showed a 30% fall in aortic pressure, a 12% rise in heart rate, and an extension of regional ischemia. The ECG showed an extension of infarct size, and CK release into the coronary vein appeared earlier than in the controls. Dogs receiving nifedipine, 1 microgram/kg, showed a 12% fall in blood pressure, no rise in heart rate, an improvement in regional perfusion, and ECG signs that suggested limitation of infarct size. There also was delayed release of coronary venous CK. The effects of nifedipine on the natural history of regional myocardial perfusion, the electrocardiogram, and enzyme release from the heart were dose related and cannot be generalized. These observations warrant further clinical investigation to improve the use of this agent in man.
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PMID:The effects of nifedipine on acute experimental myocardial ischemia and infarction in dogs. 75 29

Analog pressure signals (catheter-tip manometers) from the left atrium, left ventricle, and aorta and a flow signal from the arota were obtained in 25, open-chest, anesthetized dogs in which 115 episodes of ischemia were produced in an area of the left ventricle subtended by the distal left anterior descending coronary artery and its last major diagonal branch. The left ventricular pressure and its first derivative (dP/dt) were displayed as an X-Y loop. The character of this loop went through a unique series of dynamic changes in 110 of the 115 ischemic episodes, indicating that this is a useful tool for monitoring myocardial ischemia. Spectrum pairs of the above signals were analyzed with digital computational transfer functions in 14 ischemic episodes of three experiments and preliminary assessment reveals unique pole and zero changes in many pairs during each episode which also may prove to be a useful indicator of the hemodynamic disturbance incurred during myocardial ischemia.
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PMID:Apperceptive signals demonstrating the dynamic disturbance of myocardial ischemia. 75 16


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