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Am. J. Respir. Crit. Care Med., Vol 152, No. 6, 12 1995, 2105-2110.

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

M Okada, C Yamashita, M Okada and K Okada
Department of Surgery, Kobe University School of Medicine, Japan.

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.


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