Abstract

S546 Introduction: Left lung autotransplantation (LLA) results in a chronic increase in pulmonary vascular resistance. [1] The effects of propofol anesthesia on the pulmonary circulation are controversial. In normal dogs, propofol can induce profound pulmonary vasoconstriction in the setting of acutely elevated vasomotor tone. [2] In this study, we investigated the effects of propofol anesthesia on the left pulmonary vascular pressure-flow (LPQ) relationship in chronically-instrumented dogs with elevated vasomotor tone resulting from LLA. Methods: We utilized 8 dogs that had undergone LLA 3 to 7 weeks earlier. LPQ plots were generated by continuously measuring the pulmonary vascular pressure gradient (PAP-LAP) and left pulmonary flow (LQ) during gradual ([similar]1 min) inflation of a hydraulic occuder implanted around the right pulmonary artery. In protocol 1, LPQ plots were measured in the conscious state and during the cumulative intravenous administration of propofol anesthesia (5 mg/kg bolus plus 0.25, 0.5, 1.0 mg[center dot]kg-1 [center dot]min-1 maintenance dose). In protocol 2, LPQ plots were obtained in the conscious state, following preconstriction with the thromboxane analog, U46619 ([similar]0.2 [micro sign]g[center dot]kg-1 [center dot]min-1, iv), to acutely increase pulmonary vasomotor tone, and during propofol anesthesia as described in protocol 1. Two-way ANOVA was used to assess the effects of propofol on the LPQ relationship. Values are means +/- SEM. Results: LLA resulted in a chronic increase (p < 0.01) in pulmonary vascular resistance. Compared to the conscious state, propofol anesthesia had no effect on the baseline LPQ relationship post-LLA (Figure 1). In contrast, when pulmonary vasomotor tone was acutely increased (p < 0.01) with U46619, propofol resulted in marked dose-dependent pulmonary vasoconstriction (Figure 1).Figure 1Discussion: Despite the chronic increase in pulmonary vasomotor tone post-LLA, propofol did not exert a vasodilator influence on the baseline pulmonary circulation post-LLA. However, in the setting of acutely elevated vasomotor tone, propofol induced profound dose-dependent pulmonary vasoconstriction post-LLA.

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