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• W1976688199 abstract "Background —Activation of protein kinase C–linked receptors and subsequent opening of the mitochondrial ATP-sensitive K + (mitoK ATP ) channel are crucial in preconditioning (PC). This study examined whether postinfarct ventricular remodeling interferes with the PC mechanism. Methods and Results —Two weeks before isolation of hearts, rabbits underwent a sham operation or coronary ligation (COL) to induce remodeling. Isolated buffer-perfused hearts were subjected to 30-minute global ischemia/2-hour reperfusion, and infarct size was expressed as a percentage of the left ventricle (%I/LV), from which the scarred infarct by COL was excluded. Although %I/LV was similar in sham-operated and remodeled hearts (52.9±6.5% versus 45.8±5.2%), PC with 2 episodes of 5-minute ischemia protected sham-operated but not remodeled hearts (%I/LV=18.1±2.5% versus 54.8±2.9%, P <0.05). Infusion of valsartan (10 mg · kg − 1 · d − 1 ), an angiotensin II type 1 (AT 1 ) receptor blocker, for 2 weeks after COL prevented the ventricular remodeling and preserved the response to PC (%I/LV=27.4±3.8%), although valsartan alone did not change %I/LV. Diazoxide, a mitoK ATP channel opener, protected both sham-operated and remodeled hearts (%I/LV=14.1±3.1% and 8.3±3.6%). Conclusions —The myocardium remodeled after infarction is refractory to PC, which is probably due to interruption of cellular signaling by PC upstream of mitoK ATP channels. An AT 1 receptor blocker is beneficial not only for suppression of ventricular remodeling but also for preservation of the PC mechanism." @default.
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• W1976688199 date "2000-07-25" @default.
• W1976688199 modified "2023-09-25" @default.
• W1976688199 title "Cardioprotective Mechanism of Ischemic Preconditioning Is Impaired by Postinfarct Ventricular Remodeling Through Angiotensin II Type 1 Receptor Activation" @default.
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• W1976688199 doi "https://doi.org/10.1161/01.cir.102.4.458" @default.
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