BACKGROUNDDuring cardiac arrest, the gastrointestinal tract is sensitive to ischemia. Protection of the gastrointestinal tract is a critical factor in determining prognosis following cardiopulmonary resuscitation (CPR). This study seeks to determine the extent of gastrointestinal tract injury and the potential protective effect of inducing hypothermia following a porcine cardiac arrest model and CPR.

METHODSVentricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n = 8 per group). Four minutes after ventricular fibrillation, CPR was performed. Pigs that successfully restored spontaneous circulation then received intravenous infusions of saline at either 4°C or room temperature to produce hypothermic and control conditions respectively. Serum diamine oxidase and gastrointestinal adenosine triphosphate enzyme activity were determined and histopathology of the gastrointestinal tract was performed by light microscopy and electron microscopy.

RESULTSSignificant injury of the gastrointestinal tract after CPR was found. Na(+)-K(+) and Ca(2+) adenosine triphosphate enzyme activity in the gastric tissue were significantly high in animals receiving hypothermia treatment compared to controls. Hypothermia also significantly reduced serum diamine oxidase after CPR compared to the control group. Moreover, severe injury sustained by the gastrointestinal tissue was significantly ameliorated under hypothermic conditions compared to controls.

CONCLUSIONSGastrointestinal injury and abnormal energy metabolism are strikingly evident following CPR. Hypothermia, which is induced by an infusion of 4°C saline, can rapidly reduce internal body temperature, improve energy metabolism, and ameliorate injury to the gastrointestinal mucosa after CPR.