Desflurane Increases Pulmonary Alveolar-Capillary Membrane Permeability after Aortic Occlusion-Reperfusion in Rabbits
Open Access
- 1 June 1998
- journal article
- laboratory investigations
- Published by Wolters Kluwer Health in Anesthesiology
- Vol. 88 (6) , 1524-1534
- https://doi.org/10.1097/00000542-199806000-00017
Abstract
Background: Pulmonary injury occurs after vascular surgery, with xanthine oxidase (an oxidant generator) released from reperfusing liver and intestines mediating a significant component of this injury. Because halogenated anesthetics have been observed to enhance oxidant-mediated injury in vitro, the authors hypothesized that desflurane would increase alveolar-capillary membrane permeability mediated by circulating xanthine oxidase after thoracic occlusion and reperfusion. Methods: Rabbits were assigned to one of five groups: aorta occlusion groups administered desflurane (n=14), desflurane and tungstate (xanthine oxidase inactivator, n=12), fentanyl plus droperidol (n=13), and two sham-operated groups (desflurane, n=7 and fentanyl plus droperidol, n=7). Aortic occlusion was maintained for 45 min with a balloon catheter, followed by 3 h of reperfusion. Alveolar-capillary membrane permeability was assessed by measurement of bronchoalveolar lavage fluid protein. Xanthine oxidase activity was determined in plasma and lung tissue. Ascorbic acid content (an antioxidant) was determined in lung tissue. Results: Desflurane was associated with significantly increased alveolar-capillary membrane permeability after aortic occlusion-reperfusion when compared with the fentanyl plus droperidol anesthesia or sham-operated groups (P < 0.05). Inactivation of xanthine oxidase abrogated the alveolar-capillary membrane compromise associated with desflurane. Although significantly greater than for sham-operated animals, plasma xanthine oxidase activities released after aortic occlusion-reperfusion were not different between the two anesthetics. There were no anesthetic-associated differences in lung tissue xanthine oxidase activity. However, desflurane anesthesia resulted in a significant reduction in lung ascorbic acid after aortic occlusion-reperfusion compared with the sham-operated animals. Conclusions: Desflurane anesthesia increased xanthine oxidase-dependent alveolar-capillary membrane compromise after aortic occlusion-reperfusion in concert with depletion of a key tissue antioxidant.Keywords
This publication has 31 references indexed in Scilit:
- Lung injury after hepatoenteric ischemia-reperfusion: role of xanthine oxidase.American Journal of Respiratory and Critical Care Medicine, 1996
- Gastric intramucosal pH and multiple organ injuryCritical Care Medicine, 1996
- Effect of Volatile Anesthetics on Hydrogen Peroxide-induced Injury in Aortic and Pulmonary Arterial Endothelial CellsAnesthesiology, 1996
- Xanthine oxidase inactivation attenuates postocclusion shock after descending thoracic aorta occlusion and reperfusion in rabbitsThe Journal of Thoracic and Cardiovascular Surgery, 1995
- The Pathophysiology of Aortic Cross-clamping and UnclampingAnesthesiology, 1995
- Halothane-Oxidant Interactions in the Ex Vivo Perfused Rabbit Lung Fluid Conductance and Eicosanoid ProductionAnesthesiology, 1993
- Gut Ischemia Mediates Lung Injury by a Xanthine Oxidase-Dependent Neutrophil MechanismJournal of Surgical Research, 1993
- Experience with 1509 patients undergoing thoracoabdominal aortic operationsJournal of Vascular Surgery, 1993
- Binding of human xanthine oxidase to sulphated glycosaminoglycans on the endothelial-cell surfaceBiochemical Journal, 1993
- Halothane and Isoflurane Increase Pulmonary Artery Endothelial Cell Sensitivity to Oxidant-mediated InjuryAnesthesiology, 1991