The effect of sodium nitroprusside (SNP) on the pulmonary vasoconstrictor response to alveolar hypoxia was assessed by measuring the redistribution of blood flow in response to unilateral hypoxia. Ten dogs were anesthetized with thiopental and pentobarbital and a double-lumen endotracheal tube was inserted to permit separate ventilation of right and left lungs. Tidal volumes were maintained constant and redistribution of blood flow to each lung was followed by recording the radioactivity of mixed expired gas during the continuous intravenous infusion of 133Xe.
The pulmonary vasoconstrictor response was tested by ventilating the left lung with oxygen, 7 per cent, followed by 100 per cent nitrogen before, during and after an intravenous infusion of SNP. The experimental sequence was then repeated. Unilateral hypoxia consistently decreased blood flow to the hypoxic lung (P<0.02), and there was no significant difference in flows during nonhypoxic conditions. Following infusion of SNP at a rate sufficient to decrease the mean arterial pressure to 80 torr there was a significant increase in flow (P<0.01) to the nonhypoxic lung in response to both degrees of hypoxia. The second infusion of SNP blunted the pulmonary vasoconstrictor response to anoxia (P<0.001), but the first infusion produced no significant blunting of response to either level of hypoxia. Arterial oxygen tension values increased significantly (P<0.05) during hypoxic conditions following SNP infusion and were significantly decreased (P<0.05) during the second infusion of SNP.
These results suggest that SNP may increase arterial hypoxemia by depressing the homeostatic diversion of blood flow away from hypoxic areas of the lung; on discontinuation of SNP, there may be an increased protective response to hypoxia.