Abstract
Discussion and Conclusions
There is renewed interest in the possible effects of hypoxia upon pulmonary capillary permeability to protein in connection with the pathogenesis of high altitude pulmonary edema (6). This study was initiated partly to test the question of whether hypoxia of degrees compatible with survival of an animal did or did not induce pulmonary edema while pressure conditions were held constant. The results reported indicate that hypoxia at even lower levels of oxygen tension do not promote pulmonary edemogenesis. Haddy et al. (7) found that pulmonary edema occurred in intact dogs breathing low oxygen mixtures only when left atrial pressure was elevated. They ascribed the edemogenic effect of hypoxia in the intact dog to left ventricular failure with its consequent hydrodynamic pressure effects.
There is also a possible effect of hypoxia in the intact animal which would involve the liberation of vasoactive substances which might influence pulmonary capillary filtration pressure. Edema might be induced by pulmonary venoconstriction by such agents. Kuida et al. (8) showed that the pulmonary capillary pressure as measured by the pulmonary artery wedge method in the bovine is increased at high altitude in brisket disease. Aviado (9) showed an increase in pulmonary artery wedge pressure in hypoxia in dogs. Gilbert et al. (10) have demonstrated that epinephrine, norepinephrine, histamine, and 5-hydroxytryptamine at appropriate dose levels cause pulmonary venoconstriction in isolated perfused lungs and could therefore under some circumstances induce pulmonary edema.
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