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|Title:||The stunned myocardium: effect of electrical and mechanical arrest and osmolarity.|
|Authors:||Nayler, W G;Elz, J S;Buckley, D J|
|Affiliation:||Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.|
|Citation:||The American Journal of Physiology; 255(1 Pt 2): H60-9|
|Abstract:||After relatively short periods of ischemia, reperfusion for several hours, or even days, is required to facilitate complete recovery of the ATP stores and mechanical function. The term "stunned" has been applied to these hearts. In the present experiments, isolated, spontaneously beating and electrically paced rat hearts were made ischemic for 10 min and then reperfused with Krebs-Henseleit buffer (KH) for up to 30 min. On reperfusion, functional recovery was impaired and the inotropic effect of Ca2+ blunted. In these experiments, the effect of a period of electrical and/or mechanical quiescence before the ischemic episode was investigated. Electrical quiescence was obtained by raising the KH K+ concentration, whereas mechanical without electrical quiescence was obtained by lowering the KH Ca2+ concentration or adding 2,3-butanedione monoxime (BDM). Mechanical arrest caused by low Ca2+ perfusion before ischemia failed to improve functional recovery on reperfusion. However, introducing a high K+ perfusate or BDM for a few minutes before ischemia significantly improved the recovery during reperfusion. This improvement was neither caused by energy preservation nor an altered "reflow area". The improvement may be caused by the increased osmolarity of KH containing high K+ or BDM, since adding 10 mM sucrose to KH for an equivalent time before ischemia improved recovery and abolished the blunted inotropic effect of Ca2+.|
|Internal ID Number:||3394826|
Dose-Response Relationship, Drug
Myocardial Contraction.drug effects
Rats, Inbred Strains
|Appears in Collections:||Journal articles|
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