Halothane anesthesia causes active flow-independent pulmonary vasoconstriction

We utilized multipoint pulmonary vascular pressure-flow (P/Q̇) plots to investigate the effects of halothane anesthesia on the pulmonary circulation. Our first objective was to assess the extent to which the P/Q̇ relationship measured in conscious dogs is altered during halothane anesthesia. P/Q̇ plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q̇. Compared with conscious dogs, halothane (~ 1.2% end-tidal) resulted in active, flow-independent pulmonary vasoconstriction (P < 0.01) at all levels of Q̇. Halothane also decreased (P < 0.01) systemic arterial pressure and Q̇. Thus our second objective was to determine whether the halothane-induced pulmonary vasoconstriction was mediated by reflex neurohumoral activation or by metabolites of the cyclooxygenase pathway. However, the magnitude of halothane-induced pulmonary vasoconstriction was not significantly reduced by sympathetic α-adrenoreceptor block, angiotensin converting-enzyme inhibition, combined arginine vasopressin V₁ + V₂ receptor block, or by cyclooxygenase inhibition. Finally, halothane-induced pulmonary vasoconstriction (P < 0.01) was also observed when compared with pentobarbital-anesthetized dogs during controlled ventilation. Thus, compared with the conscious state, halothane anesthesia causes active flow-independent pulmonary vasoconstriction that is not mediated by reflex neurohumoral activation, by metabolites of the cyclooxygenase pathway, nor is it due to the effects of general anesthesia and controlled ventilation.