Effect of Estrogen on Mitochondrial Function and Intracellular Stress Markers in Rat Liver and Kidney following Trauma-Hemorrhagic Shock and Prolonged Hypotension

摘要

Traumatic hemorrhage followed by resuscitation is often fatal in civilian and military trauma, affecting organs including the liver, kidney, heart and lung. Deleterious effects of trauma-hemorrhage are influenced by sex hormones, and estrogen (E2) improves immune and cardiovascular response parameters. However, the precise mechanism by which estrogen and other sex hormones produce beneficial effects has yet to be determined. In order to target the possible early E2-mediated effects, Kozlov et al. investigated whether oxidativeitrosylative/endoplasmic reticulum (ER) stress or altered mitochondrial function are involved in prolonged hypotension and whether E2 affects these biochemical processes. Results indicate that trauma-hemorrhage followed by prolonged hypotension significantly affects mitochondrial function, ER stress markers, and free iron levels, and that E2 ameliorated these changes. E2 appears to be a hormonal adjunct that could be slow the progression of trauma-hemorrhage during patient transport to the hospital.