Human and animal experiments have not consistently shown halothane to inhibit hypoxic pulmonary vasoconstriction (HPV). The authors used a canine lung lobe perfusedin situto more precisely characterize the effects of halothane on HPV. The pulmonary vasculature can be divided into inflow, middle, and outflow segments by sequentially occluding the lobar inflow and outflow of blood. The lobes were ventilated with four different gas mixtures (normoxia, hypoxia, normoxia/halothane, hypoxia/halothane) and measured inflow, outflow, and middle segment (Rm) resistances using this stopflow technique. All values are shown as means ± standard deviation. The authors found that hypoxia increased Rm from normoxia values of .006 ± .005 cmH2O&OV0312;ml−1&OV0312; min−1to .025 ± .008 cmH2O &OV0312; ml−1&OV0312; min−1(P< 0.05). During hypoxia/halothane Rm returned to .005 ± .004 cmH2O &OV0312; ml−1&OV0312; min−1. The relationship between pressure and flow (P-&OV0312;) for the lobes for each gas mixture was also determined. The slopes of the P-&OV0312; lines by linear regression were all similar. The zero-flow pressure intercepts of the P-&OV0312; lines for normoxia (3.2 ± .9 cmH2O) and hypoxia (4.4 ± 1.1 cmH2O) were significantly decreased after the administration of halothane (1.7 ± 1.0 cmH2O and 2.6 ± 1.0 cmH2O, respectively). Since the zero-flow intercept likely reflects the tone at alveolar vessel level, the authors conclude that halothane inhibits HPV by decreasing the tone in the middle vascular segment.