Relative roles of prostaglandins and leukotrienes in canine hypoxic pulmonary vasoconstriction.

We indirectly examined the role of prostaglandins and leukotrienes in modulation of hypoxic pulmonary vasoconstriction. We used a cyclo-oxygenase inhibitor (indomethacin) and a lipoxygenase inhibitor (diethylcarbamazine) in an in-situ canine lung lobe preparation. We measured total resistance in two control groups ventilated with either 35% O2 or 3% O2 (groups CC and HC respectively). Two additional groups treated with indomethacin (groups CI and HI), and two groups treated with the combination of indomethacin and diethylcarbamazine (groups CID and HID), were also ventilated with either 35% O2 or 3% O2 respectively. Total resistance was significantly greater in hypoxic groups compared with their respective control oxygen groups. Total resistance was greatest in group HI (0.288 +/- 0.103 cm H2O.ml-1 min-1), intermediate in group HID (0.153 +/- 0.016 cm H2O.ml-1 min-1) and lowest in group HC (0.066 +/- 0.017 cm H2O.ml-1 min-1). We concluded that cyclo-oxygenase blockade augments hypoxic pulmonary vasoconstriction by decreasing production of a vasodilating prostaglandin. Hypoxia also increases production of a vasoconstricting leukotriene in the presence of cyclo-oxygenase blockade with indomethacin.