The nonpeptide endothelin receptor antagonist bosentan enhances myocardial recovery and endothelial function during reperfusion of the ischemic rat heart

J Cardiovasc Pharmacol. 1995:26 Suppl 3:S445-7.

Abstract

We investigated the effects of bosentan, a nonpeptide endothelin (ET) receptor antagonist, on ET-induced changes in coronary flow and myocardial ischemic and reperfusion injury in the isolated rat heart. Bosentan (10(-5) M ) attenuated coronary constriction induced by ET-1 and dilatation induced by the ETB agonist IRL 1620. In hearts subjected to 30 min of global ischemia followed by 30 min of reperfusion, bosentan (10(-5) M) significantly improved the recoveries of the left ventricular developed pressure, dP/dtmax, and coronary flow at the end of reperfusion, compared to vehicle-treated controls. During reperfusion, left ventricular end-diastolic pressure was significantly lower in the bosentan group than in the vehicle group. Acetylcholine-induced, endothelium-dependent vasodilatation was significantly attenuated at the end of reperfusion in controls but not in bosentan-treated hearts. We conclude that bosentan reduces myocardial and endothelial injury after ischemia/reperfusion in the isolated rat heart, indicating a pathophysiologic role of endogenous ET.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bosentan
  • Coronary Circulation / drug effects
  • Endothelin Receptor Antagonists*
  • Endothelins / pharmacology
  • Endothelium, Vascular / drug effects*
  • Heart / drug effects*
  • Male
  • Myocardial Ischemia / drug therapy*
  • Myocardial Ischemia / physiopathology
  • Myocardial Reperfusion
  • Rats
  • Rats, Sprague-Dawley
  • Sulfonamides / therapeutic use*

Substances

  • Endothelin Receptor Antagonists
  • Endothelins
  • Sulfonamides
  • Bosentan