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October 15, 2006
2:00 PM - 4:00 PM
Room Hall E, Area L
Lung Injury after Lower Body Ischemia and Reperfusion: A Comparison of Sevoflurane vs. Propofol
Thorsten Annecke, M.D., Jens Kubitz, M.D., Iris Bittmann, M.D., Gregor Kemming, M.D., Peter Conzen, M.D.
Clinic of Anesthesiology, Ludwig-Maximilians-University, Munich, Bavaria, Germany
Respiratory failure after major vascular surgery requiring temporary aortic cross clamp is not uncommon. Lower body ischemia and subsequent reperfusion trigger an inflammatory reaction involving production of cytokines, thromboxane A2 and oxygen radicals. These processes may lead to subsequent neutrophile granulocyte and platelet activation. This again induces remote organ damage, also involving the lung and especially the pulmonary vascular system. Halogenated anesthetics have been shown to reduce ischemic injury in the myocardium by a preconditioning like effect, and to reduce leukocyte-endothelium interaction during reperfusion. Thus, halogenated anesthetics may also attenuate lung injury following lower body ischemia. Since intravenous anesthesia with propofol and sevoflurane are widely used for vascular surgical procedures, we compared the effects of these anesthetics on lung injury in a porcine model of severe lower body ischemia and reperfusion. Material and Methods: Experiments had been approved by local animal care committees. A total of 18 pigs (25-30 kg) were anesthetised with midazolam. After instrumentation including catheters for invasive hemodynamic monitoring and aortic, pulmonary artery and portal venous ultrasonic flow-probes, animals were randomised to receive either sevoflurane or propofol in an investigator blinded fashion (n=9 in each group). Lower body ischemia was induced by inflating a balloon-catheter in the descending thoracic aorta. Ischemia lasted for 90min. After 120min of reperfusion, anesthesia was again switched to midazolam and continued for the remaining 180min of the investigation. Fentanyl for analgesia was given throughout the experiments. To achieve hemodynamic stability during the reperfusion period, a goal-directed resuscitation protocol (infusion of saline solution, vasopressors, buffer) was established. Arterial and mixed venous blood samples were collected to assess oxygenation and to calculate intrapulmonary shunt fraction. At the end of the experiment, a broncho-alveolar lavage was performed. Number and type of alveolar cells was assessed and total protein content and lactate dehydrogenase (LDH) activity measured in the epithelial lining fluid. Oxidative burst of alveolar macrophages was quantified using DCF (2'-7' Dichloroflourescein) - FACS analysis. To quantify edema formation, the wet to dry ratio was calculated. Morphologic lung injury was determined using a semi quantitative score by a blinded pathologist. Ten animals (n=5 for each anesthetic) without aortic occlusion served as time controls (non occlusion animals). Results: Arterial pO2 and oxygenation index decreased significantly in both anesthetic groups following reperfusion. This was accompanied by a significant increase in intrapulmonary shunt fraction. There were no significant differences between sevoflurane and propofol regarding morphologic damage score, wet to dry ratio, bronchial lavage total-protein and LDH content, or alveolar macrophage oxidative burst intensity. Neither oxygenation nor the other parameters were changed in the non-occlusion animals. Conclusion: Descending aortic occlusion and reperfusion resulted in moderately impaired pulmonary gas exchange function within the observation period of our animal study. Severity of lung injury was not different between sevoflurane and propofol.

Anesthesiology 2006; 105: A730