Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1 levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1 following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1 elevations associated with arrhythmias must result from myocardial damage to DC cardioversion.
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PMID:Direct current cardioversion. Effect on creatine kinase, lactic dehydrogenase and myocardial isoenzymes. 57 71

Myocardial ischemic injury after temporary occlusion of the left anterior descending coronary artery (LAD) for 90 min followed by reperfusion was estimated from the epicardial ST-segment elevation 15 min after occlusion (ST15m), changes in QRS complex, myocardial creatine kinase (CPK) activity and nitro-blue-tetrazolium (NBT) staining at 24 hours. At all sites exhibiting ST15m greater than 2 mV, there was a small development of epicardial Q waves after 90 min of occlusion (sigma deltaQ = 6.94 +/- 0.52 mV) and was maintained for 24 hours. Good correlations were obtained between CPK activity at 24 hours and the development of Q waves at 24 hours as well as at 60 min after reperfusion (r = 0.49; N = 56). Pretreatment with UM-272 significantly reduced the development of Q-waves (sigma deltaQ1hr = 2.23 +/- 0.75 mV) which was correlated with less CPK depletion and smaller infarct size as determined on the bais of NBT staining for myocardial tissue dehydrogenases at 24 hours. It appears, therefore, that the assessment of pathoologic Q wave development provides an accurate and early estimate of the extent of the ultimate cardiac damage due to ischemia and that pretreatment with UM-272 exerts a protective effect on the ischemic myocardium.
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PMID:Effects of dimethyl propranolol (UM-272; SC-27761) on myocardial ischemic injury in the canine heart after temporary coronary artery occlusion. 62 63

To determine whether the extensive myocardial injury associated with cardiogenic shock in some patients results from a progressive rather than a discrete massive insult, a study was made of 15 selected patients who had cardiogenic shock within 48 hours of admission, 5 patients with hypovolemic shock without myocardial infarction and 11 patients with myocardial infarction without shock. Peak plasma MB creatine kinase (CK) activity was significantly higher in the seven patients with cardiogenic shock associated with initial infarction (213 international units [IU]/liter) than in patients with shock and previous infarction (98 IU/liter) and in patients with uncomplicated myocardial infarction (125 IU/liter). A prolonged time to peak MB CK activity (averaging 26 hours) and a plateau of elevated MB CK activity were seen in patients with shock associated with initial infarction. Because shock itself did not slow the rate of apparent MB CK disappearance, results obtained suggest that cardiogenic shock associated with initial infarction in selected patients results from progressive myocardial damage underlying continuing release of MB CK into the circulation. The findings are compatible with the concept that, in these patients, cardiogenic shock reflects a vicious cycle of spreading myocardial injury, progressive compromise of cardiac function, exacerbation of ischemia and perpetuation of myocardial damage.
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PMID:Progressive nature of myocardial injury in selected patients with cardiogenic shock. 62 24

Three cases of rhabdomyolysis, two with acute renal failure, seen in a short period of time in an emergency department illustrate this increasingly recognized entity. Myoglobinuria may result from muscle trauma, ischemia, metabolic causes, drug-induced injury or intrinsic muscle disorders. The diagnosis is easily made by the presence of an elevated creatine phosphokinase, positive orthotoluidine in the urine and pigmented urine casts. Failure to diagnose rhabdomyolysis early will result in increased morbility and mortality from subsequent hyperkalemia, acute renal failure and hypocalcemia. These three cases illustrate the difficulty in predicting the eventual degree of renal failure from the initial assessment.
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PMID:Rhabdomyolysis and acute renal failure. 63 72

The results of experiments with indirect methods have suggested that various interventions reduce infarct size after coronary artery occlusion. To determine and quantify directly both the short- and long-term effects of several interventions on myocardial salvage without relying on indirect methods, the left coronary artery was occluded in 880 rats; they were then given either no treatment or one of the following interventions: (a) hyaluronidase, an enzyme that hydrolyzes interstitial glycoproteins, 1,500 National Formulary (NF) U/kg i.v. 5 min and 24 h after occlusion; (b) cobra venom factor, a protein that depletes the third component of complement, 20 U/kg i.v. 5 min after occlusion; (c) a glucocorticoid: hydrocortisone, 50 mg/kg i.v. 5 min after occlusion; or the five-fold more potent methylprednisolone (MP): (i) 50 mg/kg i.v. 5 min after occlusion or (ii) 50 mg/kg i.v. 5 min after occlusion followed by 50 mg/kg i.m. 3, 6, and 24 h after occlusion; or (d) reserpine, an agent that depletes the heart of catecholamines, 0.5 mg/kg i.m. once on each of the 3 days before occlusion. The animals were sacrificed either 2 days after occlusion, i.e., at the time of peak necrosis, or after 3 wk, i.e., after the infarct was completely healed. The amount of preserved myocardium was then assessed by two independent techniques: planimetric measurement of serial histologic sections and creatine kinase activity of the whole left ventricle. The amount of normal myocardium preserved at 21 days postocclusion was significantly increased, by 22.3+/-7.8% (P < 0.025) after the administration of hyaluronidase, by 25.3+/-5.8% (P < 0.005) after cobra venom factor, by 14.5+/-6.9% (P < 0.05) after hydrocortisone, by 20.8+/-8.2% (P < 0.025) after the single dose of MP, by 20.9+/-3.9% (P < 0.001) after the four doses of MP, and by 10.2+/-3.7% (P < 0.05) as a result of pretreatment with reserpine. The four doses of MP significantly thinned the infarct-by 25.6+/-2.9% (P < 0.001)-and although ventricular rupture did not occur, the intervention caused distension of the left ventricle as a result of stretching of the infarcted tissue during scar formation. Thus, myocardium acutely jeopardized by ischemia can be preserved on a long-term basis.
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PMID:Long-term preservation of ischemic myocardium after experimental coronary artery occlusion. 64 Nov 37

To determine whether nifedipine, a calcium antagonist, protects ischemic myocardium, conscious dogs were subjected to coronary occlusion and given nifedipine by intravenous infusion beginning 30 minutes after the onset of ischemia and lasting for 24 hours while systemic arterial pressure, left atrial pressure, and cardiac output were monitored. Local myocardial perfusion at selected intervals after coronary occlusion was assessed with radioactive microspheres injected into the left atrium. In regions of myocardium exhibiting moderately depressed flow 29 minutes after occlusion in control dogs (n = 8), flow was significantly greater 3 and 23.5 hours later, reflecting increases in collateral perfusion. Corresponding zones of myocardium in treated dogs (n = 9) exhibited significantly greater increases in flow at each interval after occlusion (P less than 0.05). Furthermore, myocardial creatine kinase depletion (which correlated well with morphometric estimates of necrosis) in myocardium matched for ischemia prior to treatment was 1.5 to 3 times less in treated than in control dogs (P less than 0.05). Thus, nifedipine produced sustained increases in collateral flow and reduced myocardial ischemic injury.
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PMID:Effects of nifedipine on myocardial perfusion and ischemic injury in dogs. 67 20

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

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 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

It has been proposed that a single preoperative dose of a corticosteroid may protect the myocardium from ischemic injury during open heart surgery. To test this hypothesis, a prospective, randomized, double blind study was carried out in ninety-five patients undergoing coronary bypass surgery using intermittent ischemic arrest with systemic and local hypothermia. Half the patients received 2 gm (approximately 30 mg/kg) of methylprednisolone 2 hours prior to the initiation of cardiopulmonary bypass and the other half received a placebo. Postoperative electrocardiograms and blood levels of serum creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and serum glutamic oxalacetic transaminase (SGOT) were compared in the two groups. No apparent difference was noted in the number of patients with significantly elevated levels of CPK, LDH, or SGOT or in the number with positive isoenzyme patterns of CPK and LDH. Moreover, there was no significant difference in the mean values of CPK, LDH, or SGOT between the two groups. The number of patients with electrocardiographic evidence of myocardial injury (10 per cent) was the same in both groups and no difference was noted in (1) the ease with which patients could be weaned from cardiopulmonary bypass, (2) postoperative arrhythmias, (3) postoperative bleeding, (4) postoperative respiratory insufficiency, and (5) length of hospital stay. It is concluded that a single preoperative dose of 2 gm of methylprednisolone offers no demonstrable protection to the myocardium from the effects of ischemia during coronary artery bypass surgery.
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PMID:Effect of methylprednisolone on myocardial preservation during coronary artery surgery. 77 98


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