Effects of anoxic or oxygenated reperfusion in globally XXXX , isovolumic, perfused @entity35 hearts.

@entity296 @entity1568 @entity63 @entity39 @entity908 @entity26 @entity10943 @entity35
It has not previously been possible to study the in vitro effects of reperfusion on severely injured isolated perfused hearts because of the development of the no-reflow phenomenon, concomitant with the onset of irreversible @entity296 . A new model of @entity63 which utilizes an intraventricular balloon to allow uniform reperfusion of irreversibly damaged hearts is described. The effects of reperfusion were studied in Langendorff perfused @entity35 hearts after no-flow @entity63 for 60 and 150 minutes at 37 C. Uniform reflow was facilitated by maintaining the left ventricle at an isovolumic diastolic volume with a balloon during @entity63 and removal of the balloon prior to reflow. Reperfusion was with 1) anoxic media, 2) oxygenated media, 3) oxygenated media in the presence of the mitochondrial inhibitor Amytal, or 4) an initial anoxic reperfusion followed by oxygenated media. Injury was monitored by the assay of released @entity908 kinase (CK) and @entity10943 (Myo), by light-microscopic estimates of the percent of cells containing contraction bands, and by ultrastructural changes. CK and Myo were released with anoxic reperfusion, but larger releases occurred with oxygenated reperfusion. Amytal inhibited the @entity26 but not the @entity1568 component of release. Contraction bands occurred following oxygenated, but not anoxic, reperfusions and were inhibited by Amytal. Following an initial anoxic reperfusion, @entity26 caused additional CK and Myo release and produced an increase in the percent of cells with contraction bands, compared with that with @entity26 alone. The response of cells to injury was heterogeneous, and the hearts contained cells with a spectrum of ultrastructural changes. Anoxic reperfusion was associated with cellular swelling and oxygenated reperfusion with contraction band @entity39 .
