Brief pressure overload preconditions rabbit myocardium independent of adenosine receptor activation

Background: We previously reported brief pressure overload of the left ventricle reduced myocardial infarct size. The role of adenosine receptors was investigated in this study.

Methods: 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.

Results: 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.

Conclusions: 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.