Halothane anesthesia abolishes pulmonary vascular responses to neural antagonists

We investigated the effects of the inhalational anesthetic halothane on autonomic nervous system (ANS) regulation of the baseline pulmonary vascular pressure-flow (P/Q̇) relationship compared with that measured in the conscious state. Multipoint pulmonary vascular P/Q̇ plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q̇. P/Q̇ plots were generated in the same dogs in the conscious state and during halothane anesthesia (~1.2% end tidal) in the intact (no drug) condition and after administration of selective ANS antagonists. In conscious dogs, sympathetic α₁-adrenoreceptor block with prazosin decreased (P<0.01) the pulmonary vascular pressure gradient [pulmonary arterial pressure-pulmonary arterial wedge pressure (PAP-PAWP)] over the entire range of Q̇ studied; i.e., inhibition of endogenous α₁-adrenoreceptor activity caused pulmonary vasodilation. In contrast, α₁-adrenoreceptor block had no effect on PAP-PAWP at any value of Q̇ during halothane anesthesia. In conscious dogs, sympathetic β-adrenoreceptor block with propranolol increased (P<0.01) PAP-PAWP over the entire range of Q̇ studied; i.e., inhibition of endogenous β-adrenoreceptor activity resulted in pulmonary vasoconstriction. However, β-adrenoreceptor block had no effect on PAP-PAWP at any value of Q̇ during halothane anesthesia. Finally, cholinergic receptor block with atropine decreased (P < 0.05) PAP-PAWP at values of Q̇ > 100 ml·min^-1·kg^-1 in conscious dogs but had no effect on PAP-PAWP at any value of Q̇ during halothane anesthesia. These results indicate that endogenous ANS regulation of the baseline pulmonary vascular P/Q̇ relationship observed in conscious dogs is abolished during halothane anesthesia.