Moderate XXXX initiated during oxygen-glucose deprivation preserves HL-1 cardiomyocytes.

@entity1 @entity1545 @entity522 @entity353 @entity130 @entity23258 @entity519 @entity2332 @entity2383
OBJECTIVES: @entity2332 ( @entity2332 ) is an acknowledged strategy for neuroprotection for @entity1 suffering from @entity1545 ( @entity1545 ). Albeit similar pathomechanisms of @entity1545 for both brain and heart, moderate @entity2332 (32-34  C) has not been established as a heart-protective measure. Therefore, we investigated the cardioprotective effects of moderate @entity2332 on oxygen-glucose deprivation/re-oxygenation ( @entity23258 /R)-induced @entity130 . METHODS: @entity519 was induced by exposing HL-1 cardiomyocytes to 0.2% oxygen in serum/glucose-free medium for 6h. @entity23258 injured cells were subsequently re-oxygenated with 21% oxygen in complete medium. Two hypothermic protocols were investigated: Post- @entity23258 cooling to 33.5  C for 24h initiated at the start of re-oxygenation and intra- @entity23258 cooling to 33.5  C for 24h initiated after 3h of @entity23258 and maintained throughout the re-oxygenation phase. Cell viability was determined by LDH and cTnT releases. Mitochondria dysfunction was evaluated by intracellular ATP content and cellular metabolic activity was accessed by MTT reduction. Activation of @entity522 was analyzed by Western blot. RESULTS: @entity23258 /R-induced injury resulted in increased cell death (higher LDH and cTnT releases), @entity2383 (decreased ATP content), and decreased cellular metabolic activity ( @entity353 ). Only intra- @entity23258 cooling attenuated both @entity23258 and @entity23258 -R-induced @entity130 (significantly decreased LDH and cTnT releases and increased ATP contents and MTT reduction). Furthermore, @entity522 activation was abated by intra- @entity23258 cooling. No protective effects were observed by post- @entity23258 cooling. CONCLUSIONS: Moderate @entity2332 initiated during @entity23258 is a promising intervention for the protection of cardiomyocytes from @entity23258 /R-induced injury. The attenuation of @entity2383 and apoptosis by intra- @entity23258 cooling are beneficial effects of @entity2332 -induced cardioprotection, resulting in minimized myocardial cell death after @entity23258 and @entity23258 -R-induced @entity130 .
