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'' horm one that is known to play a key role in cardiovascular homeostasis of the systemic circulation. In contrast, the effects of AVP on the pulmo nary circulation have not been extensively investigated, and the exten t to which general anesthesia alters the pulmonary vascular response t o AVP is entirely unknown. Our first objective was to assess the effec ts of AVP on the pulmonary vascular pressure-flow relation in chronica lly instrumented conscious dogs in the setting of an acute elevation i n pulmonary vasomotor tone. Our second objective was to investigate th e effects of halothane and pentobarbital anesthesia on the pulmonary v ascular response to AVP after inducing the same degree of pulmonary pr econstriction achieved in the conscious state. Methods: Conditioned, m ongrel dogs were chronically instrumented to measure the left pulmonar y vascular pressure-flow (LPQ) relation. LPQ plots were generated by c ontinuously measuring the pulmonary vascular pressure gradient (pulmon ary arterial pressure minus left atrial pressure) and left pulmonary b lood flow during gradual (similar to 1 min) inflation of a hydraulic o ccluder around the right pulmonary artery, which directed total pulmon ary blood flow through the left pulmonary circulation. LPQ plots were generated in conscious (n = 10), halothane-anesthetized (n = 9) and pe ntobarbital-anesthetized (n = 7) dogs. In each condition, LPQ plots we re 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 pr econstriction. Results: U46619 caused acute pulmonary vasoconstriction (P < 0.01) in conscious dogs. In this setting of U46619 preconstricti on, AVP caused pulmonary vasodilation (P < 0.05) in the conscious stat e. In contrast, despite identical levels of U46619 preconstriction, th e pulmonary vasodilator response to AVP was either reversed to vasocon striction (P < 0.05) or abolished during halothane and pentobarbital a nesthesia. Conclusions: These results Indicate that AVP exerts a signi ficant pulmonary vasodilator response in the setting of acute pulmonar y vasoconstriction in conscious dogs. However, the pulmonary vascular response to this stress hormone is markedly altered during halothane a nd pentobarbital anesthesia.