Thyroid influence in reactions to O2 at atmospheric pressure

Publisher Website
Google Scholar
Abstract
Experiments were carried out to determined what effect increased thyroid might have on the reactions induced in normal and hypophysectomized rats by continuous exposure to O2 at atmospheric pressure (OAP). Feeding desiccated thyroid or injecting thyroxine increased the noxious effects of OAP. The data support the interpretation a) that the development of hypercapnemia and hypooxemia secondarily to the initial pulmonary damage (probably induced by O2, per se, or in combination with small amounts of CO2) is rapidly increased by thyroid; b) that this further aggravates the initial pulmonary damage by direct action on the pulmonary vasculature and indirectly by central stimulation of the sympatho-adrenomedullary and hypophyseal-adrenocortical axes with a resultant release of adverse neurogenic and hormonal influence on the lungs. Other important thyroid effects which may augment the toxicity of OAP are discussed as is their possible involvement in the experimental production of hyaline membrane disease and retrolental fibroplasia. The data provide supporting evidence that the protection which hypophysectomy affords against O2 toxicity is due in part to the attendant elimination of thyrotropin and the resultant reduction of thyroid secretion.

This publication has 11 references indexed in Scilit: