Chemical preconditioning with 3-nitropropionic acid in hearts: Role of mitochondrial KATP channel

Ramzi A. Ockaili, Peeyush Bhargava, Rakesh C. Kukreja

Research output: Contribution to journalArticle

66 Scopus citations

Abstract

We investigated the cardioprotective effect of 3-nitropropionic acid (3-NPA), an inhibitior of mitochondrial succinate dehydrogenase, and we wanted to show whether this protection is mediated by of opening mitochondrial ATP-sensitive potassium (KATP) channels. Adult rabbits were treated with either 3-NPA (3 mg/kg iv) or saline (n = 6 rabbits/group). After 30 min (for early phase) or 24 h (for late phase) of the treatment, the animals were subjected to 30 min of ischemia and 3 h of reperfusion (ischemia-reperfusion). 5-Hydroxydecanoate (5-HD, 5 mg/kg iv),the mitochondrial KATP channel blocker, was administered 10 min before ischemia-reperfusion in the saline- and 3-NPA-treated rabbits. 3-NPA caused a decrease in the infarct size from 27.8 ± 4.2% in the saline group to 16.5 ± 1.0% in the 3-NPA-treated rabbits during early phase and from 30.4 ± 4.2% in the saline group to 17.6 ± 1.05 in the 3-NPA group during delayed phase (P < 0.05, % of risk area). The anti-infarct effect of 3-NPA was blocked by 5-HD as shown by an increase in infarct size to 33 ± 2.7% (early phase) and 31 ± 2.4% (delayed phase) (P < 0.05 vs. 3-NPA groups). 5-HD had no proischemic effect in control animals. Also, 3-NPA had no effect on systemic hemodynamics. We conclude that 3-NPA induces long-lasting anti-ischemic effects via opening of mitochondrial KATP channels.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number5 49-5
StatePublished - May 1 2001
Externally publishedYes

Keywords

  • Ischemia
  • Oxidative phosphorylation
  • Succinate dehydrogenase

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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