Brief pressure overload preconditions rabbit myocardium independent of adenosine receptor activation.

Abstract

We previously reported brief pressure overload of the left ventricle reduced myocardial infarct size. The role of adenosine receptors was investigated in this study. Pressure overload was achieved by two 10-minute partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Ten minutes after different pretreatments, 60-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion was done to induce infarction. The area at risk and myocardial infarct size were determined by Evans blue dye injection and triphenyltetrazolium chloride staining. Myocardial infarct size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group (19.3 ± 2.5 %, p < 0.001) and in the ischemic preconditioning group (18.3 ± 1.8 %, p < 0.001) versus the control group (27.3 ± 3.3 %). Pretreatment with 8-(p-sulfophenyl)-theophylline, an adenosine receptor antagonist, limited the protection by ischemic preconditioning (26.8 ± 3.7%), but not that by pressure overload (19.2 ± 2.5%, p < 0.001). The 8-(p-sulfophenyl)-theophylline did not significantly affect the extent of infarct (26.4 ± 5.4%). The hemodynamics prior to treatment, area at risk, and mortality were not significantly different among all groups of animals. Brief pressure overload of the left ventricle preconditioned rabbit myocardium against infarction. Because 8-(p-sulfophenyl)-theophylline had no significant effect on this response, the results are consistent with the hypothesis that the underlying mechanism does not depend on activation of adenosine receptors.