Korth Ulrike, Krieter Heiner, Denz Christof, Janke Christoph, Ellinger Klaus, Bertsch Thomas, Henn Claudia, Klein Jochen
Faculty of Clinical Medicine Mannheim, Institute of Anesthesiology, University of Heidelberg, 68165 Mannheim, Germany.
Resuscitation. 2003 Aug;58(2):209-17. doi: 10.1016/s0300-9572(03)00119-9.
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.
肠缺血是休克综合征的一种主要并发症，可导致细菌和内毒素移位以及重症监护患者发生多器官功能衰竭。本研究旨在使用微透析作为一种工具，来监测猪心脏骤停和复苏后的肠缺血情况。为此，将微透析探针植入猪的空肠壁、腹膜、骨骼肌和大脑，并在循环骤停（由室颤诱发）期间及自主循环恢复（ROSC）后获取组织间液。通过乙醇技术测定，心脏骤停4分钟导致空肠壁、肌肉和大脑中的血流长时间（60分钟）减少。这伴随着心肌和大脑中的细胞损伤，分别表现为肌钙蛋白-I和蛋白S-100水平升高。心脏骤停后15至60分钟，血浆葡萄糖、乳酸和胆碱水平升高。相比之下，心脏骤停导致所有监测器官中的组织间葡萄糖水平迅速但可变地降低；这种降低之后在再灌注期间超过基线水平而升高。在肠道中，缺血和再灌注60至120分钟期间乳酸、谷氨酸和胆碱水平升高；肠道和腹膜样本中乳酸水平呈现平行变化。大脑和肌肉样本显示出与肠道和腹膜类似的变化，但谷氨酸除外，谷氨酸在大脑中升高而在肌肉中未升高。我们得出结论，肠缺血是心脏骤停和复苏的结果，并且可以通过体内微透析进行监测。通过多部位微透析的比较分析表明，肠道对缺血的敏感性与大脑或肌肉相同，甚至更高。
