Time related changes in XXXX handling in the isolated @entity63 and reperfused @entity35 heart.

@entity308 @entity35 @entity63 @entity1426 @entity460 @entity141
The main aim of this study was to assess the kinetics of intracellular free @entity460 ( @entity141 i) handling by isolated @entity35 hearts rendered @entity63 for 30 min followed by 30 min of reperfusion analyzing the upstroke and downslope of the @entity141 i transient. Changes in mechanical performance and degradation of membrane phospholipids--estimated by tissue @entity1426 content--were correlated with @entity141 i levels of the heart. The fluorescence ratio technique was applied to estimate @entity141 i. The disappearance of mechanical activity of the heart preceded that of the @entity141 i transient in the first 2 min of @entity63 . The slope of upstroke of the @entity141 i transient, reflecting @entity141 release, decreased by 60%, while the duration of the downslope of the transient, reflecting @entity141 sequestration, expressed a significant prolongation (105 +/- 17 vs. 149 +/- 39 msec) during the first 3 min of @entity63 . At about 20 min of @entity63 end-diastolic pressure expressed a 3.5-fold increase (contracture) when the fluorescence ratio showed a 2-fold elevation. Reperfusion was accompanied with a further precipitous increase in end-diastolic pressure, while resting @entity141 i remained at end- @entity63 levels. Increases in the @entity1426 (AA) content of the @entity63 and postischemic hearts were proportional to @entity141 i levels. In summary, the present findings indicate that both @entity460 release and removal are hampered during the early phase of @entity63 . Moreover, a critical level of @entity141 i and a critical duration of @entity63 may exist to provoke contracture of the heart. Upon reperfusion the hearts show membrane phospholipid degradation and signs of stunning exemplified by elevated AA levels, partial recovery of @entity141 i handling and sustained @entity308 of mechanical performance.
