Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits

Yumin Qiu, Ali Rizvi, Xian Liang Tang, Srinivas Manchikalapudi, Hitoshi Takano, Asad K. Jadoon, W. U. Wen-Jian, Roberto Bolli

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138 Scopus citations

Abstract

-We tested the hypothesis that late precondi-tioning (PC) against myocardial infarction is triggered by the formation of nitric oxide (NO). Conscious rabbits underwent a 30-min coronary occlusion followed by 3 days of reperfusion. In group I (control group, n = 10), rabbits were not preconditioned, whereas in group II (n -10), they were preconditioned 24 h earlier with a sequence of six 4-min occlusion/4min reperfusion cycles. Myocardial infarct size (tetrazolium staining) was reduced by 50% by PC (28.6 ±3.2% of the risk region in group II vs. 56.9 ±5.9% in controls, P < 0.05). This reduction in cell death was associated with improved recovery of myocardial function [ systolic thickening fraction (by sonomicrometry) at 3 days 2.0 ±11.0% of baseline in group II vs. -20.0 ±2.8% in groupl, P < 0.05]. Group ///rabbits (n = 11) underwent the same protocol as group II except that the rabbits received the NO synthase inhibitor Nω-nitro-L-arginine (L-NNA, 13 mg/kg) before the PC ischemia. In these animals, infarct size did not differ significantly from that observed in control rabbits, indicating that L-NNA completely blocked the development of late PC against myocardial infarction. In group IV (: n = 9, rabbits received L-NNA as in group HI, but without the six occlusion-reperfusion cycles, and were subjected to the 30-min occlusion 24 h later. In this group, infarct size did not differ from that observed in controls, demonstrating that pretreatment with L-NNA, in itself, did not affect the extent of cell death. Taken together, these results indicate that, in the conscious rabbit, the development of late PC against myocardial infarction is triggered by the generation of NO during the PC ischemia. It is proposed that NO plays a key role in the delayed myocardial adaptation to ischémie stress.

Original languageEnglish (US)
Pages (from-to)H2931-H2936
JournalAmerican Journal of Physiology
Volume273
Issue number6 PART 2
DOIs
StatePublished - 1997

Keywords

  • L-arginine
  • Myocardial ischemia-reperfusion
  • Nitric oxide synthase
  • Nitrogen radicals
  • Oxygen radicals

ASJC Scopus subject areas

  • Physiology (medical)

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