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Article
December 1989

Development of a Bacteria-Independent Model of the Multiple Organ Failure Syndrome

Author Affiliations

From the Departments of Surgery (Drs Steinberg, Flynn, Kelley, Bitzer, Hassett, Price, and Flint, Mr Sharma, and Ms Gutierrez), Pharmaceutics (Drs Baxter and Lalka), Pathology (Dr Sands), and Medicine (Drs Van Liew and Beam), State University of New York at Buffalo and the Buffalo Veterans Administration Medical Center.

Arch Surg. 1989;124(12):1390-1395. doi:10.1001/archsurg.1989.01410120036008
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 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.

(Arch Surg. 1989;124:1390-1395)

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