Increased Pulmonary Vascular Pressor Response to Hypoxia in Highland Dogs

Greater pulmonary vascular resistance increases in response to acute hy-poxia have been observed in the anesthetized dog at 1600-m altitude than in dogs studied at sea level. Consequently, the he-modynamic response to hypoxia was studied in 11 “lowland” dogs flown to Denver and compared to the response of 11 dogs obtained locally. The local “highland” dogs had mean increases in pulmonary arterial pressure and pulmonary vascular resistance during hypoxia of +17 ± 1 mm Hg and + 5.3 ± 0.9 mm Hg/liter/min, respectively, in contrast to the increases of +12 ± 1 mm Hg and +2.8± 0.2 mm Hg/liter/min observed in the lowland dogs. The increase in pulmonary arterial pressure induced by prostaglandin F_2a was not significantly different in the two groups. The pulmonary pressor response to hypoxia in seven lowland dogs restudied after 3- to 4-weeks residence at 1600 m was not altered. The difference in responsiveness of the pulmonary vascular bed to hypoxia in the two groups suggests that chronic low-grade hypoxia may alter hypoxic reactivity, and that the resident altitude should be considered when comparing data from various laboratories. We are very grateful to Dr. A. L. Hyman and Dr. P. J. Kadowitz (Louisiana) and Dr. J. A. Will (Wisconsin) who supplied the sea level dogs for the study. Excellent technical assitance was provided by Mary Munroe, Ro-sann Glas, Steve Hofmeister, Bruce Hookway, Don Jackson, Bea Kaplan, and Eva Toyos. The manuscript was prepared by Karen Leahy. Prostaglandin F_2a was kindly supplied by Dr. John Pike, Upjohn Co., Kala-mazoo, Mich. The study was supported by NIH Grants No. HL 14985 and No. HL 05973.