Renal Hemodynamics and Prostaglandin E2 Excretion in a Nonhuman Primate Model ofSeptic Shock

摘要

Human septic shock (SS) is an important clinical problem with a high mortality.The typical hemodynamic features includes hypotension, low systemic vascular resistance (SVR), and a preserved or increased cardiac output. In addition, organ system dysfunction is common and may affect the heart, lungs, brain, and endocrine glands. Renal dysfunction is a particularly serious complication of SS and may substantially increase morbidity and mortality. However, the mechanisms responsible for renal insufficiency in SS have not been fully described. As renal perfusion pressure falls, the kidney may attempt to increase blood flow by various mechanisms. One such mechanism involves prostaglandin E2 (PGE sub 2), a potent endogeneous vasodilator which may be produced by the kidney to augment renal blood flow. However, the renal excretion of PGE sub 2 in a low SVR model of SS has not been previously measured. The purpose of this study was to determine the effects of severe SS on renal hemodynamics and on the renal excretion of PGE sub 2 in a nonhuman primate model that closely simulates human SS. Keywords: Reprints. (kr)