Pulmonary vasoregulation by arginine vasopressin in conscious, halothane-anesthetized, and pentobarbital-anesthetized dogs with increased vasomotor tone.

BACKGROUND

Arginine vasopressin (AVP) is an important "stress" hormone that is known to play a key role in cardiovascular homeostasis of the systemic circulation. In contrast, the effects of AVP on the pulmonary circulation have not been extensively investigated, and the extent to which general anesthesia alters the pulmonary vascular response to AVP is entirely unknown. Our first objective was to assess the effects of AVP on the pulmonary vascular pressure-flow relation in chronically instrumented conscious dogs in the setting of an acute elevation in pulmonary vasomotor tone. Our second objective was to investigate the effects of halothane and pentobarbital anesthesia on the pulmonary vascular response to AVP after inducing the same degree of pulmonary preconstriction achieved in the conscious state.

METHODS

Conditioned, mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relation. LPQ plots were generated by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure minus left atrial pressure) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder around the right pulmonary artery, which directed total pulmonary blood flow through the left pulmonary circulation. LPQ plots were generated in conscious (n = 10), halothane-anesthetized (n = 9) and pentobarbital-anesthetized (n = 7) dogs. In each condition, LPQ plots were measured at baseline, during the intravenous administration of the thromboxane analog U46619 and during the cumulative administration of AVP (2-19 ng.kg-1.min-1, intravenous) in the presence of U46619 preconstriction.

RESULTS

U46619 caused acute pulmonary vasoconstriction (P < 0.01) in conscious dogs. In this setting of U46619 preconstriction, AVP caused pulmonary vasodilation (P < 0.05) in the conscious state. In contrast, despite identical levels of U46619 preconstriction, the pulmonary vasodilator response to AVP was either reversed to vasoconstriction (P < 0.05) or abolished during halothane and pentobarbital anesthesia.

CONCLUSIONS

These results indicate that AVP exerts a significant pulmonary vasodilator response in the setting of acute pulmonary vasoconstriction in conscious dogs. However, the pulmonary vascular response to this stress hormone is markedly altered during halothane and pentobarbital anesthesia.