saralasin and Ventricular-Dysfunction--Left

The aim of the present study was to assess the participation of angiotensin II receptors in the triggering mechanism of ischemic preconditioning. Isolated buffer-perfused rabbit hearts were subjected to 40 min of regional ischemia (37 degrees C) followed by 60 min of reperfusion. Ischemic preconditioning was induced with three cycles of 5-min ischemia and 10-min reperfusion given prior to the 40-min ischemic period. Infarct size and ventricular function were assessed. Ischemic preconditioning reduced infarct size to 5.2 +/- 1.2% of the area at risk (mean +/- S.E.M., P<0.001) when compared to controls (26.4 +/- 3.0%), but did not protect against ventricular dysfunction. Activation of angiotensin II receptors with angiotensin II (100 nM) also limited infarct size (9.6 +/- 2.2%, P

Topics: Analysis of Variance; Angiotensin Receptor Antagonists; Animals; Biphenyl Compounds; Coronary Circulation; Drug Evaluation, Preclinical; Female; Imidazoles; In Vitro Techniques; Ischemic Preconditioning, Myocardial; Losartan; Male; Myocardial Infarction; Myocardial Reperfusion; Rabbits; Renin-Angiotensin System; Saralasin; Tetrazoles; Ventricular Dysfunction, Left