Brief left ventricular pressure overload reduces XXXX .

@entity10740 @entity296 @entity1976 @entity39 @entity2310 @entity4124 @entity1977 @entity741 @entity35 @entity583
BACKGROUND: Both apoptosis and @entity39 contribute to cell death after @entity741 and reperfusion. We previously reported that brief left ventricular pressure overload (LVPO) decreased @entity583 ( @entity583 ) size. In this study, we investigated whether brief pressure overload reduces apoptosis and the mechanisms involved. MATERIALS AND METHODS: @entity583 was induced by a 40-min occlusion of the left anterior descending coronary artery and 3-h reperfusion in male anesthetized @entity35 . Brief LVPO was achieved by two 10-min partial snarings of the ascending aorta, raising the systolic left ventricular pressure 50% above the baseline value. Ischemic preconditioning was elicited by two 10-min coronary artery occlusions and 10-min reperfusions. RESULTS: Brief LVPO and ischemic preconditioning significantly decreased @entity583 size (P  <  0.001). Brief pressure overload significantly reduced @entity296 , as evidenced by the decrease in the terminal deoxynucleotidyl transferase-mediated @entity1977 nick-end labeling-positive nuclei (P  <  0.001), little or no DNA laddering, and reduced @entity4124 activation (P  <  0.01). Moreover, brief pressure overload significantly increased @entity1976 (P  <  0.001) and decreased @entity2310 (P  <  0.001) and @entity10740 (P  <  0.01). Akt phosphorylation was significantly increased by brief pressure overload (P  <  0.001), whereas c-Jun N-terminal kinase phosphorylation was significantly decreased (P  <  0.001). Hemodynamics, area at risk, and mortality did not differ significantly among groups. CONCLUSIONS: Brief left LVPO significantly reduces @entity296 . The underlying mechanisms might be related to modulation of @entity1976 and @entity2310 , inhibition of @entity10740 , increased Akt phosphorylation, and suppressed c-Jun N-terminal kinase phosphorylation.
