Hypophyseal and Adrenocortical Factors in Pulmonary Damage Induced by Oxygen at Atmospheric Pressure

Abstract

In exposures to O2 concns. of 90% and above at atmospheric pressure and continuous absorption of CO2, nonhypophysectomized rats became dyspneic, lethargic, anorexic within 20 hrs. and continued to deteriorate to coma. Some succumbed within 45 hrs., and all were dead or sacrificed at 70 hrs. The thoraces were filled with clear watery bloodless fluid which clotted firmly on standing. Lungs were liver like in color, rubbery in consistency, devoid of air and sank in fixing soln. This massive hydrothorax helps explain the decreased vital capacity of animals exposed to O2 at atm. pressure. In contrast to these effects none of the hypophysectomized rats showed such severe effects of O2 and none succumbed before 70 hrs., although some were dyspneic. Thoraces were free of fluid and lungs appeared normal. The results confirm the authors'' earlier findings that hypophysectomy protects against pulmonary damage by O2 by eliminating or diminishing those principles which, released in the normal animal, augment the susceptibility of pulmonary tissue, particularly the vascular bed, to injurious effects of O2 in high concns. Corticotropin and cortical hormones, among them cortisone, constitute important elements of this augmentatory mechanism out are not essential to the precipitation of pulmonary injury by O2. The possibility that increased CO2 is a factor is discussed.