Does nitric oxide generation contribute to the mechanism of remote ischemic preconditioning?

N N. Petrishchev¹, T D. Vlasov, V G. Sipovsky

¹Department of Pathophysiology, St. Petersburg, I. P. Pavlov's State Medical University, Lev Tolstoy Str., 6/8, 197022/1, St. Petersburg, Russia

Pathophysiology : the Official Journal of the International Society for Pathophysiology

|March 3, 2001

Abstract:

The protective effect of local or remote ischemic preconditioning (IPC) on subsequent 40-min ischemic and 120-min reperfusion myocardial damage was investigated. Preconditioned rats underwent one cycle of myocardial ischemia/reperfusion consisting of 5-min ischemia produced as a left coronary artery (LCA) occlusion and 5 min of reperfusion. Remote IPC was produced as 15 min of small intestinal ischemia with 15 min of reperfusion as well as 30 min of limb ischemia with 15 min of reperfusion. A marked protective action was afforded by both IPC protocols with a more significant effect of local (classic) ischemic preconditioning. Since the protective effect of remote IPC was not abolished by nitric oxide (NO) synthase inhibition with Nomega-nitro-L-arginine (L-NNA) it is concluded that NO generation may not be involved in the mechanism of remote IPC.