Abstract
Gastrointestinal complications following cardiopulmonary bypass (CPB) are associated with high mortality rates. The identification of prolonged CPB time and calcium administration as independent predictors of gastrointestinal complications suggests decreased splanchnic perfusion as a possible mechanism. To test this hypothesis, we evaluated splanchnic organ perfusion during CPB and after calcium chloride administration. Mongrel dogs were studied under anesthesia and were cannulated for bypass. CPB was begun at 37°C, and the heart was fibrillated and vented. After 30 min, CPB temperature was reduced to 25°C for 1 h with the heart arrested through cold crystalloid cardioplegia. After rewarming to 37°C for 30 min, the heart was cardioverted, and CPB was weaned off. Calcium chloride (10 mg/kg) or saline was administered. Organ blood flow was determined with radiolabeled microspheres at baseline, during CPB, and after weaning from CPB. Splanchnic organ blood flow did not decrease during any phase of CPB. Calcium chloride administration after CPB had no effect on splanchnic organ blood flow. While gastrointestinal injury may result from CPB, this study suggests that the mechanism of injury is not decreased by splanchnic organ perfusion during bypass. While calcium chloride can cause pancreatic injury, the responsible mechanism is not calcium-induced hypoperfusion.
Published Version
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