Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subendocardial ischemia develops in hearts that are fibrillated during cardiopulmonary bypass when: (1) the normal ventricle is fibrillated with a sustained electrical stimulus, (2) the hypertrophied ventricle is allowed to fibrillate spontaneously, (3) the fibrillating heart becomes distended, or (4) the perfusion pressure is reduced to approximately 50 mm Hg. Myocardial hypothermia reduces cardiac oxygen requirements during fibrillation but does not prevent ischemia when perfusion pressure falls to levels frequently attained during clinical open-heart operations. The ischemia occurs because flow cannot rise sufficiently to meet the metabolic demands of ventricular fibrillation. The forces interacting to impede adequate flow to the subendocardium during ventricular fibrillation are: (1) the compressive forces exerted on subendocardial muscle by the strength of fibrillation, (2) the compressive forces resulting from raised intracavitary pressure due to occlusion or malfunction of the ventricular vent, and (3) the evolution of myocardial edema as ischemia is prolonged. We have abandoned the use of ventricular fibrillation in clinical open-heart operations and now allow the heart to beat continually with adequate perfusion pressure. We have not needed to use inotropic drugs postoperatively after aortic or mitral valve replacement since adopting this technique.
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PMID:Ventricular fibrillation. Its effect on myocardial flow, distribution, and performance. 80 60

Subendocardial ischemia is a common cause of death following ischemic cardiac arrest. We studied relationships among myocardial water content (WC), left ventricular function, coronary blood flow, and myocardial metabolism following ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia, 120 min of aortic occlusion was employed, and myocardial temperature was kept around 20 degrees C in 10 mongrel dogs. Left ventricular function (peak LVP, max dp/dt, LVEDP, LVSWI), coronary blood flow, myocardial enzymes (m-GOT, total CPK, MB-CPK), myocardial ATP and creatine phosphate (CP), and WC of the subendocardium of the left ventricle were measured. Data were obtained in the control state and immediately and 30 and 60 min after aortic unclamping. Significant negative correlations were obtained between WC and max dp/dt (r = -0.8384), coronary blood flow (r = -0.9928), ATP (r = -0.7038), and CP (r = -0.7835). Significant positive correlations were obtained between WC and LVEDP (r = 0.7525), m-GOT (r = 0.7638), and total CPK (r = 0.7079). These data suggest that myocardial edema results in depression of left ventricular function and metabolism.
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PMID:Correlation among water content, left ventricular function, coronary blood flow, and myocardial metabolism after hypothermic ischemic cardiac arrest. 685 73