Intestinal ischaemia during cardiac arrest and resuscitation: comparative analysis of extracellular metabolites by microdialysis.

Intestinal ischaemia is a major complication of shock syndromes causing translocation of bacteria and endotoxins and multiple organ failure in intensive care patients. The present study was designed to use microdialysis as a tool to monitor intestinal ischaemia after cardiac arrest and resuscitation in pigs. For this purpose, microdialysis probes were implanted in pig jejunal wall, peritoneum, skeletal muscle and brain, and interstitial fluid was obtained during circulatory arrest (induced by ventricular fibrillation) and after return of spontaneous circulation (ROSC). Cardiac arrest for 4 min caused a prolonged (60 min) reduction of blood flow in jejunal wall, muscle and brain as determined by the ethanol technique. This was accompanied by cellular damage in heart muscle and brain as indicated by increased levels of troponin-I and protein S-100, respectively. Plasma levels of glucose, lactate and choline were increased at 15-60 min following cardiac arrest. In contrast, cardiac arrest induced a rapid but variable decrease of interstitial glucose levels in all monitored organs; this decrease was followed by an increase over baseline during reperfusion. In the intestine, lactate, glutamate and choline levels were increased during ischaemia and reperfusion for 60-120 min; intestinal and peritoneal samples yielded parallel changes of lactate levels. Brain and muscle samples showed similar changes as in intestinum and peritoneum except for glutamate, which was increased in brain but not in muscle. We conclude that intestinal ischaemia occurs as a consequence of cardiac arrest and resuscitation and can be monitored by in vivo microdialysis. Comparative analysis by multi-site microdialysis reveals that the intestine is equally or even more sensitive to ischaemia than brain or muscle.