Simultaneous Ca2+ imaging and electrophysiological analysis demonstrate source of Ca2+ for EAA receptors.
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Biomedical subjects
Publications and source records attributed to A Abbott.
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Accidental hypothermia due to exposure is an infrequent cause of circulatory arrest. A premature diagnosis of clinical death must be avoided in these patients and vigorous attempts at active rewarming are indicated. Extracorporeal circulation in the form of partial cardiopulmonary bypass has been reported as an effective means of rapid, even core rewarming. We wish to report a recent case at Ruby Memorial Hospital in which extracorporeal circulation was used successfully in resuscitating a profoundly hypothermic multi-trauma victim.
Hypercalcemic reperfusion of the postischemic heart has been associated with ventricular dysfunction and with ultrastructural changes in the mitochondria. The isolated working rat heart model was used to correlate ventricular function, mitochondrial damage, and high-energy phosphate content with degree and timing of hypercalcemia during reperfusion. When administered early during reperfusion, calcium chloride caused a dose-dependent deterioration in ventricular function, whereas calcium augmented function when it was administered after a 15-minute period of normocalcemic reperfusion. Hearts treated with calcium early during reperfusion demonstrated more mitochondrial damage and decreased stores of adenosine triphosphate than those in which calcium administration was delayed. The data indicate that a period of normocalcemic reperfusion should precede calcium administration in the postischemic heart. Mitochondrial damage resulting in decreased synthesis of adenosine triphosphate is likely the cause of ventricular dysfunction associated with calcium administration in the postischemic heart.
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