Effect of hypertransfusion on the gastrointestinal tract after cardiac arrest in a porcine model.

Abstract

This study aimed to determine the potential protective effect of inducing hypertransfusion to the gastrointestinal tract following a porcine model of cardiac arrest and cardiopulmonary resuscitation (CPR) by evaluating the influence of gastrointestinal ultrastructure, ATPase and serum diamine oxidase. Ventricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n=8/group). Four minutes after ventricular fibrillation, CPR was performed. The pigs that successfully restored spontaneous circulation received intravenous infusion of either norepinephrine to maintain the mean arterial pressure at 130% of the baseline before ventricular fibrillation or normal saline. Serum diamine oxidase and gastrointestinal ATPase activity were determined, and histopathological examination of the gastrointestinal tract was performed by light and electron microscopy. CPR caused significant injury to the gastrointestinal tract, elevating serum diamine oxidase and causing destruction of intestinal microvillus in control animals. Na(+)-K(+) ATPase and Ca(2+) ATPase activity in gastric tissue were significantly elevated in animals receiving hypertransfusion treatment compared with the control animals. Hypertransfusion also significantly reduced serum diamine oxidase to below control levels after CPR. Moreover, severe injury sustained by the gastrointestinal tissue was markedly ameliorated under hypertransfusion conditions compared with the control animals. Gastrointestinal injury and abnormal energy metabolism were strikingly evident following CPR. Hypertransfusion inducing hypertension can improve energy metabolism and ameliorate gastrointestinal mucosal injury, indicating that hypothermia significantly ameliorates gastrointestinal injury sustained following cardiac arrest.