Autonomic nervous system pulmonary vasoregulation after hypoperfusion in conscious dogs

We investigated the role of the autonomic nervous system (ANS) in the pulmonary vascular response to increasing cardiac index after a period of hypoperfusion (defined as reperfusion) in conscious dogs. Base-line and reperfusion pulmonary vascular pressure-cardiac index (P/Q̇) plots were generated by stepwise constriction and release, respectively, of an inferior vena caval occluder to vary Q̇. Surprisingly, after 10-15 min of hypoperfusion (Q̇ decreased from 139 ± 9 to 46 ± 3 ml·min^-1·kg^-1), the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) was unchanged over a broad range of Q̇ during reperfusion compared with base line when the ANS was intact. In contrast, pulmonary vasoconstriction was observed during reperfusion after combined sympathetic β-adrenergic and cholinergic receptor block, after β-block alone, but not after cholinergic block alone. The pulmonary vasoconstriction during reperfusion was entirely abolished by combined sympathetic α- and β-block. Although sympathetic α-block alone caused pulmonary vasodilation compared with the intact, base-line P/Q̇ relationship, no further vasodilation was observed during reperfusion. Thus the ANS actively regulates the pulmonary circulation during reperfusion in conscious dogs. With the ANS intact, sympathetic β-adrenergic vasodilation offsets α-adrenergic vasoconstriction and prevents pulmonary vasoconstriction during reperfusion.