Contribution of endothelin-1 to warm ischemia/reperfusion injury of the rat lung

Am J Respir Crit Care Med. 1995 Dec;152(6 Pt 1):2105-10. doi: 10.1164/ajrccm.152.6.8520782.

Abstract

The purpose of the present study was to clarify the role of endothelin-1 (ET-1) in the pathogenesis of ischemia/reperfusion lung injury and to determine whether pretreatment with an ET receptor antagonist prevents such injury. The left lung of Sprague-Dawley rats was subjected to 60 min of no-flow warm ischemia followed by 90 min of reperfusion. The plasma ET-1 concentration increased significantly after reperfusion compared with before and after ischemia (p < 0.05). Arterial oxygen tension was reduced, and the lung tissue wet/dry weight ratio increased in post-reperfusion lungs compared with both pre-ischemia and post-ischemia lungs. Histologic study showed pulmonary edema, hemorrhage, hyaline membrane formation, and a significant increase in lung tissue neutrophils after reperfusion. In addition, the expression of ET-1 mRNA was determined by Northern blot analysis. Although ischemia did not significantly alter ET-1 expression, reperfusion increased expression in the left lung markedly and in the right lung moderately. Pre-infusion of FR139317, an ETA receptor antagonist, prevented post-reperfusion damage to the lung. These results suggest that ET-1 contributes to the ischemia/reperfusion injury of the rat lung, mediated by an ETA receptor, and that an ETA receptor antagonist may inhibit ischemia/reperfusion lung injury.

MeSH terms

  • Animals
  • Azepines / pharmacology
  • Blotting, Northern
  • Endothelin Receptor Antagonists
  • Endothelins / blood
  • Endothelins / genetics
  • Endothelins / physiology*
  • Indoles / pharmacology
  • Lung / blood supply*
  • Lung / pathology
  • Male
  • Organ Size
  • Oxygen / blood
  • RNA, Messenger / analysis
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / blood
  • Reperfusion Injury / pathology
  • Reperfusion Injury / physiopathology*

Substances

  • Azepines
  • Endothelin Receptor Antagonists
  • Endothelins
  • Indoles
  • RNA, Messenger
  • FR 139317
  • Oxygen