HEPARAN PRESERVES INTESTINAL PERFUSION AFTER HEMORRHAGE AND RESUSCITATION

Background: Multiple system organ failure (MOF) remains a major source of morbidity and mortality in trauma patients. Despite restoration of central hemodynamics, intestinal hypoperfusion can persist. Mucosal i schemia and barrier breakdown are factors in the genesis of MOF. Hepar an sulfate is a gycosaminoglycan similar to heparin, but with minimal anticoagulant properties. As an adjunct to resuscitation, it improves immunologic function and restores mucosal oxygenation and function. We hypothesized that resuscitation with heparan following hemorrhage wou nd prevents intestinal hypoperfusion. Materials and methods: In vivo v ideomicroscopy was used to study small intestine microcirculation in r ats. Animals were hemorrhaged to 50% of baseline mean arterial pressur e (MAP) and maintained there. Resuscitation was initiated when the ret urn of 10% shed blood was required to beep MAP at 50%. Animals receive d either heparan (7 mg/kg/l mi saline) or saline (1 mi) followed by th e remaining shed blood and an equal volume of saline. MAP, cardiac out put (GO), Al arteriole diameters, and how were determined. Results: Re suscitation of the saline control group resulted in normal MAP with el evation of CO to 25-40% above baseline. The heparan group had return o f MAP but only a moderate increase in CO (7-15%). Saline resuscitation led to progressive deterioration in Al diameters and how. The additio n of heparan prevented delayed Al constriction and significantly impro ved perfusion. Conclusions: Heparan prior to resuscitation improved in testinal perfusion, despite a relative reduction in CO. Improvement in nutrient blood how may protect the mucosal barrier, reducing the inci dence of MOF, and suggests that heparan may be useful in resuscitation of trauma patients. (C) 1996 Academic Press