Ischemic Postconditioning Protects Against Global Cerebral Ischemia/Reperfusion-Induced Injury in Rats

Abstract

Background and Purpose-Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats. Methods-Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats.

Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage

“…16 Experimental and clinical studies have indicated the protective effects of postconditioning in ischaemia/reperfusion injury. [17][18][19][20][21] This protection is not only associated with inhibition of inflammation and apoptosis, 22,23 but also with attenuation of oxidative stress. 3,24 The aim of the present study was to use a rat model of ischaemia/ reperfusion injury to evaluate the effects of ischaemic postconditioning on mitochondrial ROS production, in order to determine whether its inhibitory effects on oxidative stress are mediated via the mitochondrial pathway, since the golgi apparatus is also a source of ROS.…”

Preconditioning and postconditioning: from bench to bedside

“…(35) Providing the IPost protocol is modifi ed appropriately, most animal hearts appear amenable to IPost, including human myocardium. (36,37) Other organs in which IPost has reported to be benefi cial include, the brain, (38) kidney (39) and liver. (by echocardiography) at one year.…”

Post-conditioning with gradually increased reperfusion provides better cardioprotection in rats

“…The total time from ischemia to post-conditioning differed between the two algorithms, with the routine algorithm lasting 10 seconds (5 cycles of 10 seconds reperfusion/ischemia) and the modified algorithm lasting 140 seconds (15/20-20/15-25/10-30/5 seconds). In a study of post-conditioning after brain ischemia, Wang et al [17] discovered that when the time of brief reperfusion was too long and the ischemia time was too short (3 cycles of 60/15 seconds of reperfusion/re-occlusion), the protective effect was attenuated or even lost.…”