Mechanisms of the coronary vasoconstriction induced by high
arterial oxygen tension .
Mouren, St[acute]ephane, Rachid Souktani, Marc Beaussier, Lamine
Abdenour, Martine Arthaud, Michel Duvelleroy, and Eric Vicaut.
Laboratoire de Biophysique, H[circumflex]opital Fernand Widal and
Unit[acute]e 141 Institut National de la Sant[acute]e et de la
Recherche M[acute]edicale, 75010 Paris, France; and
D[acute]epartement d'Anesth[acute]esie-R[acute]eanimation and
Laboratoire des Urgences, H[circumflex]opital Piti[acute]e
-Salp[acute]etri[grave]ere, Paris, France
APStracts 3:0296H, 1996.
In isolated rabbit hearts perfused with suspension of red blood cells,
we investigated the role of the endothelium and of several substances
in the coronary vasoconstriction induced by a high arterial blood
oxygen tension (PaO2). Red blood cells in Krebs-Henseleit buffer were
oxygenated to obtain control and high PaO2 perfusates. Arterial
oxygen content was kept constant in both perfusates by reducing
hemoglobin concentration in the high PaO2 perfusate. Coronary blood
flow was kept constant so that O2 supply would not vary with the rise
in PaO2. Increases in perfusion pressure therefore reflected
increased coronary resistance. The high PaO2-induced coronary vaso
constriction was not affected by administration of indomethacin,
nordihydroguaiaretic acid, NG-nitro-L-arginine or superoxide
dismutase and catalase but was abolished after endothelium damage or
by cromakalim. These results demonstrate that 1) the endothelium
contributes to the high PaO2-induced coronary vasoconstriction 2)
this effect is independent of cyclooxygenase or lipoxygenase
products, nitric oxide or free radicals 3) the closure of KATP
channels mediates this vasoconstriction.
Received 20 December 1995; accepted in final form 28 June 1996.
APS Manuscript Number H1186-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996