Multipoint pulmonary vascular pressure/flow relationships in hypoxic and in normoxic dogs: effects of nitrous oxide with and without cyclooxygenase inhibition.

The authors investigated the effects of 70% nitrous oxide on overall mean pulmonary artery pressure (MPAP)/cardiac index (CI) relationships in 13 intact pentobarbital anesthetized dogs ventilated alternatively in normoxic (fraction of inspired O2, FIO2 0.3) and in hypoxic (FIO2 0.1) conditions. Five-point MPAP/CI plots were constructed by opening an arterio-venous femoral fistula or by stepwise inflations of a balloon in the inferior vena cava. These MPAP/CI plots were rectilinear in all experimental conditions. Over the entire range of CI studied, 1-5 l.min-1.m-2, hypoxia increased MPAP in seven dogs ("responders"), and did not affect MPAP in six other dogs ("nonresponders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in "nonresponders" by administration of 1 g acetylsalicylic acid (ASA) intravenously. In "responders," nitrous oxide partially inhibited HPV. In "nonresponders" with a hypoxic pressor response restored by ASA, nitrous oxide enhanced both normoxic and hypoxic pulmonary vascular tone, and did not affect HPV. These results suggest that pulmonary vascular effects of nitrous oxide depend on preexisting pulmonary vascular tone, and may be modulated by cyclooxygenase products of arachidonic acid metabolism.