Hormone changes and beta-endorphin in the pathogenesis of hemorrhagic shock

Plasma levels of some hormones, implicated in the pathogenesis of hypovolemic shock (ACTH, corticosterone, plasma renin activity, aldosterone, prostaglandins, vasopressin and beta-endorphin) were examined on rats with hemorrhagic shock. The animals were treated with the specific opioid antagonist, naloxone (1 mg/kg body weight, i. v.). The results demonstrated that during the first, compensated stage of hypovolemic shock, an increase of ACTH, corticosterone, vasopressin, and stimulation of renin-angiotensin-aldosterone system was evident, that is, an activation of hormonal mechanisms responsible for blood pressure and blood volume restoration occurred. beta-Endorphin and prostaglandin E-release during hemorrhagic shock might contribute to the cardiodepressor changes. Naloxone treatment prevented the development of shock into a progressive stage by several eventual mechanisms: An antagonism of opiate receptors. Stimulation of ACTH secretion, followed by an increased secretion of glucocorticoids or a direct effect on adrenocortical function. Stimulation of aldosterone secretion by ACTH or directly.