Endothelin receptor antagonist SB209670 decreases lung allograft apoptosis and improves lung graft function after prolonged ischemia

J Cardiovasc Pharmacol. 2000 Nov;36(5 Suppl 1):S209-11. doi: 10.1097/00005344-200036051-00063.

Abstract

Apoptosis has been postulated as a contributing factor in ischemia-reperfusion graft dysfunction following lung transplantation. The purpose of this study was to determine whether treatment with an endothelin-A/endothelin-B- (ET(A)/ET(B)) receptor antagonist could reduce the level of apoptosis observed in the lung following ischemia-reperfusion injury. Eleven dogs were subjected to left lung allotransplantation. Heart-lung blocks were harvested from donor dogs and preserved with modified Eurocollins solution and stored at 4 degrees C for 18 to 20 h. We investigated the level of apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), in the lungs of animals receiving an intravenous infusion of saline (control, n = 5) or the ET receptor antagonist SB209670 (n = 6) (15 microg/kg/min). The infusion began 30 min prior to transplantation and continued for up to 6 h thereafter. The TUNEL staining was significantly higher in the airway epithelium and the parenchyma of the saline (control) group (40.67 +/- 6.16), compared with native right lungs (5.00 +/- 0.56) and the treatment group (14.13 +/- 2.84). We conclude that treatment of lung allografts with the mixed ET(A)/ET(B)-receptor antagonist SB209670 can ameliorate lung injury by reducing the level of apoptosis seen in the allograft following ischemia-reperfusion injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Dogs
  • Endothelin Receptor Antagonists*
  • In Situ Nick-End Labeling
  • Indans / pharmacology*
  • Ischemia / physiopathology*
  • Lung / blood supply*
  • Lung / pathology
  • Lung / physiopathology
  • Lung Transplantation / adverse effects*
  • Transplantation, Homologous

Substances

  • Endothelin Receptor Antagonists
  • Indans
  • 1H-Indene-2-carboxylic acid, 1-(1,3-benzodioxol-5-yl)-3-(2- (carboxymethoxy)-4-methoxyphenyl)-2,3-dihydro-5-propoxy-, (1S,2R,3S)-