Pulmonary vascular responses to acute hypoxia.

Abstract

The role of the respiratory gases in the regulation of the pulmonary circulation has been a major area of research in respiratory physiology since von Euler and Liljestrand demonstrated in 1946 that changes in the composition of the inspired gas can alter the pulmonary arterial pressure (12). Hypoxia plays a particularly important role in the fine regulation of the pulmonary circulation. The effects of hypoxia on the pulmonary circulation became of increasing theoretical and practical concern consequent to the development of pulmonary function tests, the widened use of general (i.e., gas) anesthesia, the application of gas isotope technics, and the advent of high atmospheric and space flights (12, 25, 26). The recently proposed theory of the “Pulmonary Hypoperfusion Syndrome” relates fetal hypoxia to changes in the pulmonary vascular bed and alveolar metabolism of the fetus (7, 9). A large volume of physiologic data on hypoxia is now available, well summarized by Fishman in 1961 (13). Significant physiologic contributions have appeared in the literature since 1961 (22–24; 30–32) but few attempts have been made to correlate the physiologic data with the radiologic and arteriographic studies (1, 34, 36). The purpose of the present project was to analyze in vivo morphologic changes—demonstrated angiographically—underlying the physiologic events which accompany acute hypoxia. Material and Methods Experiments were performed in 10 adult mongrel dogs, weighing 33–39 lb. Intravenous Diabutal—1 cc per 5 lb.—was used for anesthesia. Cut-downs were performed on the groins. The femoral arteries were cannulated with gray Kifa catheters and utilized for arterial blood sampling and pressure recording. Control studies were performed as follows: right heart and pulmonary artery catheterizations were carried out with No. 8 Rodriguez-Alvarez catheters, and pulmonary wedge catheterization with No. 6 Cournand and Lehman catheters. Left atrial catheterization was achieved by the transseptal approach, using a No. 18 Brockenbrough needle and yellow Kifa catheters. Cardiac outputs were measured by the standard dye dilution technic, using indocyanine green. No ectopic beats were detected during cardiac output determination. All pressures were recorded via Statham transducers on an Electronic for Medicine physiologic recorder. Pulmonary resistance was calculated in units, using the formula where R = resistance, P.A.P. = mean pulmonary artery pressure in mm Hg, L.A.P. = mean left atrial pressure in mm Hg, and Q = cardiac output in L∕min. Pulmonary arteriography was performed using 35 cc of sodium iothalamate, injected in one and a half seconds through a No. 8 Rodriguez-Alvarez catheter with a Cordis pressure injector.