Combined Therapy for Combined Injury: Modulation of iNOS Induced Inflammatory Cyt

Office Of The Director, National Institutes Of Health

Investigators

Abstract

Nearly 40% of the causalities after a nuclear detonation will sustain combined injury, burns and/or wounds in addition to radiation exposure, siginificantly increasing their risk of morbidity and mortality. Hemorrhage further increases these risks. Animal studies clearly demonstrate that burns and wounds exacerbate the acute radiation syndrome. Data from humans similarly demonstrates that burns and wounds complicate the morbidity and mortality of personnel exposed to ionizing radiation. The mechanisms of this interaction are unknown. Radiation injury, wounds and burns, and other stressful conditions all result in the release of cell mediators that complicate recovery of cell renewal systems of the skin, bone marrow and the gut. Complications in recovery of cell renewal systems lead to delayed and ineffective (a) healing of the tissue trauma, (b) marrow cell recovery, and (c) intestinal cell repopulation. These complications increase the probability of death from sepsis. Radiation also directly damages proliferative cell systems of the skin, marrow, and the gut leading to increased risks from subsequent sepsis.