Opposing effects of isoflurane and sevoflurane on neurogenic pulmonary edema development in an animal model
Opposing effects of isoflurane and sevoflurane on neurogenic pulmonary edema development in an animal model
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DOI：
10.1097/00000542-200506000-00018
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发表时间：
2005-06-01
期刊：
影响因子：
8.8
通讯作者：
Ishikawa, N
中科院分区：
文献类型：
--
作者：
Kandatsu, N;Nan, YS;Ishikawa, N
背景资料：本研究旨在探讨异氟醚和七氟醚预处理对大鼠神经源性肺水肿（neurogenic pulmonary edema，NPH）的影响。方法：将大鼠分别暴露于室内空气（control）、1.5%异氟醚和2.5%七氟醚中4 h。然后，他们与戊巴比妥钠腹腔注射麻醉，纤维蛋白原和凝血酶注入枕大池，以诱导神经源性pulmonary edema.Results：纤维蛋白原和凝血酶的连续注射引起血压升高，与峰值在异氟烷和七氟烷组获得低于对照值。对照组、异氟烷组和七氟烷组中显著神经源性肺水肿的发生率分别为58%、100%和8%。对照组、异氟烷组和七氟烷组的肺水比（水肿严重程度的指数）分别为4.86 +/- 0.78、6.15 +/- 0.64和4.40 +/- 0.32。此外，血管内皮生长因子的免疫组织化学染色表明，在暴露于异氟烷的大鼠肺中表达增加。在暴露于异氟烷的过程中，用抗血管内皮生长因子抗体治疗完全抑制了异氟烷促进神经源性肺水肿在此模型中的作用。结论：暴露于1.5%异氟烷增强了神经源性肺水肿在此动物模型中的发展，最有可能是通过释放血管内皮生长因子从支气管上皮细胞，没有观察到与七氟烷的效果。
Background: The current study was undertaken to investigate the effects of pretreatment with isoflurane and sevoflurane on the development of neurogenic pulmonary edema in an animal model.Methods: Rats were exposed to room air (control), 1.5% isoflurane, or 2.5% sevoflurane for 4 h. They were then anesthetized with intraperitoneal injections of pentobarbital sodium, and fibrinogen and thrombin were injected into the cisterna magna to induce neurogenic pulmonary edema.Results: Consecutive injections of fibrinogen and thrombin caused increases in blood pressure, with the peak values obtained in the isoflurane and sevoflurane groups being lower than the control values. The incidence of significant neurogenic pulmonary edema was 58%, 100%, and 8% in the control, isoflurane, and sevoflurane groups, respectively. The lung water ratio, an index of severity of edema, was 4.86 +/- 0.78, 6.15 +/- 0.64, and 4.40 +/- 0.32 in the control, isoflurane, and sevoflurane groups, respectively. Furthermore, immunohistochemical staining for vascular endothelial growth factor demonstrated an increase of expression in the rat lungs exposed to isoflurane. Treatment with an anti-vascular endothelial growth factor antibody during exposure to isoflurane completely inhibited the effect of isoflurane to promote neurogenic pulmonary edema in this model.Conclusion: Exposure to 1.5% isoflurane enhances the development of neurogenic pulmonary edema development in this animal model, most likely via release of vascular endothelial growth factor from bronchial epithelial cells, an effect not observed with sevoflurane.