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多器官功能障碍综合征非细菌依赖模型的建立。

Development of a bacteria-independent model of the multiple organ failure syndrome.

作者信息

Steinberg S, Flynn W, Kelley K, Bitzer L, Sharma P, Gutierrez C, Baxter J, Lalka D, Sands A, van Liew J

机构信息

Department of Surgery, State University of New York, Buffalo.

出版信息

Arch Surg. 1989 Dec;124(12):1390-5. doi: 10.1001/archsurg.1989.01410120036008.

DOI:10.1001/archsurg.1989.01410120036008
PMID:2589963
Abstract

Criteria that allow definition of the multiple organ failure syndrome include pulmonary, hepatic, renal, and gut barrier dysfunction along with characteristic histopathologic changes. It has been difficult to study multiple organ failure due to lack of a satisfactory experimental model that would reproduce the pathophysiologic and histopathologic characteristics, would be stable enough to allow study over several days, and would be free of exogenous primary bacterial infection. We have studied pathophysiologic and histopathologic alterations in a potential model of multiple organ failure. Wistar rats received one of the following solutions by intraperitoneal injection: 4 mL of saline, 4 mL of mineral oil, or 1 mg per gram of body weight of zymosan A in 4 mL of mineral oil. Animals that received zymosan developed hypoxia, decreased creatinine clearance, and changes in hepatic microsomal cytochrome P450 content and aniline hydroxylase activity. Bacterial translocation occurred in the zymosan group. The lungs, liver, and kidneys of the animals that received zymosan exhibited histopathologic changes. We conclude that this model fulfills our criteria for a model of multiple organ failure.

摘要

能够定义多器官功能衰竭综合征的标准包括肺、肝、肾和肠道屏障功能障碍以及特征性组织病理学变化。由于缺乏一个能重现病理生理和组织病理学特征、足够稳定以便进行数天研究且无外源性原发性细菌感染的满意实验模型,多器官功能衰竭的研究一直很困难。我们研究了一个潜在的多器官功能衰竭模型中的病理生理和组织病理学改变。Wistar大鼠通过腹腔注射接受以下溶液之一:4毫升生理盐水、4毫升矿物油或每克体重1毫克酵母聚糖A溶于4毫升矿物油中。接受酵母聚糖的动物出现缺氧、肌酐清除率降低以及肝微粒体细胞色素P450含量和苯胺羟化酶活性的变化。酵母聚糖组发生了细菌移位。接受酵母聚糖的动物的肺、肝和肾出现了组织病理学变化。我们得出结论,该模型符合我们对多器官功能衰竭模型的标准。

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