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)

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

The effect of acute myocardial ischemia on the myocardial elastic modulus has been a matter of controversy. To evaluate this question, diastolic elastic modulus was assessed by finite element analysis of left ventricular geometry using three-dimensional echocardiographic reconstructions and right and left ventricular pressure recordings. Elastic properties were estimated before and after coronary occlusion in 6 open-chest dogs. Elastic modulus values were derived by means of a computer program that determined the global elastic modulus that best predicted the diastolic changes in left ventricular geometry. In the finite element analysis after coronary occlusion, two analyses were performed: one utilizing the control elastic modulus for all segments of the left ventricle and one in which ischemic (dyskinetic) segments were assigned a higher elastic modulus. Results showed that the control elastic modulus was a poor predictor of diastolic left ventricular expansion after coronary occlusion. The finite element analysis in which the ischemic segments were assigned a higher elastic modulus better predicted ischemic diastolic wall motion patterns. Error values (difference between predicted and actual left ventricular segmental diastolic motion) were: control, 1.9 +/- 0.3 mm (mean +/- SD), ischemia, 2.9 +/- 0.5 mm, and 2.2 +/- 0.4 mm using the stiffer elastic modulus for ischemic segments. Error values were significantly higher (p less than 0.05) under ischemic conditions when the control elastic modulus was uniformly applied compared with control and ischemia with dyskinetic segments assigned a higher elastic modulus. From these data, it is concluded that the myocardial diastolic elastic modulus is increased by ischemia and that this approach may allow clinical assessment of intrinsic muscle stiffness.
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PMID:Finite element analysis of myocardial diastolic function using three-dimensional echocardiographic reconstructions: application of a new method for study of acute ischemia in dogs. 359 46

Serum creatine kinas (C.K.), aspartate amino-transferase (G.O.T.), and alkaline phosphatase (A.P.) activities were measured in 211 men with serum cholesterol concentrations in the upper one-third of the normal distribution. Of these, 110 were receiving clofibrate and 101 were given identical capsules containing olive oil. These investigations were also carried out on 85 healthy men with low serum cholesterol levels not receiving clofibrate.No differences were observed in C.K. and G.O.T. activities between any of these groups; A.P. was significantly lower in the clofibrate-treated group. No significant alterations in C.K. occurred during serial observations made in 15 patients with ischaemic heart disease over a period of five months. No instance of myalgia or muscle stiffness was recorded in 452 men who had received clofibrate for one year.It is concluded that raised C.K. and G.O.T. concentrations and the occurrence of myalgia are uncommon accompaniments of clofibrate treatment.
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PMID:Clofibrate, serum enzymes, and muscle pain. 542 Feb 39