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- W1570661302 abstract "Introduction: Both apoptosis and necrosis contribute to cell death after myocardial ischemia and reperfusion. We previously reported brief left ventricular pressure overload decreased myocardial infarct (MI) size. Hypothesis: We investigated whether pressure overload reduces apoptosis and the mechanisms involved. Methods: MI was induced by 40-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion in anesthetized Sprague-Dawley rats. Brief left ventricular pressure overload was achieved by two episodes of 10-minute partial snaring of the ascending aorta, raising the systolic left ventricular pressure 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions and 10-mintue reperfusion. Results: Brief left ventricular pressure overload as well as ischemic preconditioning significantly decreased MI size (p Conclusions: Thus, brief left ventricular pressure overload significantly reduces apoptosis. The underlying mechanisms might be related to modulation of expression of Bcl-2 and Bax, inhibition of p53, increase of Akt phosphorylation, and suppression of JNK phosphorylation." @default.
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- W1570661302 date "2014-11-25" @default.
- W1570661302 modified "2023-09-24" @default.
- W1570661302 title "Abstract 169: Brief Left Ventricular Pressure Overload Reduces Apoptosis After Myocardial Ischemia and Reperfusion" @default.
- W1570661302 hasPublicationYear "2014" @default.
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