Cyclooxygenase inhibition and effects of hypoxia on pulmonary circulation and gas exchange in anesthetized dogs

Respiration Physiology
H ShamsJ Piiper

Abstract

To investigate whether endogenously produced prostanoids are involved in hypoxic pulmonary vasoconstriction, pulmonary hemodynamic and gas exchange parameters and eicosanoid metabolites were measured in 5 anesthetized, artificially ventilated dogs (mean body weight 27 kg). Hypoxia elicited pulmonary vasoconstriction, but blood plasma levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F 1 alpha (6kPGF1 alpha) (stable metabolites of TXA2 and prostaglandin I2, respectively) remained unchanged. Administration of the cyclooxygenase inhibitor indomethacin blocked the synthesis of prostanoids, so that 6kPGF1 alpha and TXB2 levels decreased to values below the detection level (10 pg.ml-1) both during normoxia or hypoxia, but did not affect pulmonary vascular resistance or the alveolar-arterial PO2 difference (PAi-Pa)O2. The pulmonary vascular bed remained, however, responsive to TXA2 as evidenced by infusion of the TXA2 mimetic, U 46619, which significantly increased the pulmonary vascular resistance and (PAi-Pa)O2. Our data suggest that prostanoids are not involved in eliciting the effects of hypoxia on pulmonary hemodynamics and gas exchange efficiency.

Citations

Aug 1, 1991·Respiration Physiology·J P RichaletP Rémy
Mar 1, 1992·Respiration Physiology·D W SheehanL E Farhi
Oct 1, 1993·Respiration Physiology·D W Sheehan, L E Farhi
Nov 1, 1990·American Journal of Respiratory Cell and Molecular Biology·T R MurrayE J Macarak
Nov 23, 2013·Journal of Veterinary Cardiology : the Official Journal of the European Society of Veterinary Cardiology·Alexandre Le RouxLorrie Gaschen

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