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RICHARD C. LILLEHEI, M.D.; LLOYD D. MacLEAN, M.D.

AMA Arch Surg. 1959;78(3):464-471.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

The gravity of Gram-negative bacteremia has long been recognized,^1,2 but it is only recently that the lethal effect of these organisms when present in the systemic circulation has been correlated with their ability to produce shock³. The ability to cause shock in man, as well as in a variety of laboratory animals, is apparently dependent upon a lipoprotein-carbohydrate complex, or endotoxin, which is liberated at death from the cell wall of the Gram-negative bacteria.⁴ While the mechanism by which endotoxin causes shock is not clear, there is increasing evidence that its faculty of causing profound vasospasm in the small blood vessels^5,6 is intimately linked with its capacity to cause shock. In the dog, hemoconcentration, plasma loss, increased plasma hemoglobin, bloody diarrhea, and hemorrhagic necrosis of the bowel mucosa regularly follow the injection of endotoxin and are apparently the result of the vasospastic effect of endotoxin . . . [Full Text PDF of this Article]

Author Affiliations
St. Paul

From the Department of Surgery, University of Minnesota Medical School and Ancker Hospital Research Laboratory.

Footnotes
Submitted for publication June 24, 1958.

Supported by Grant #2941 from the U. S. Public Health Service and a grant from the Louis W. and Maud Hill Family Foundation.

Read before the Section on Pathology and Physiology at the 107th Annual Meeting of the American Medical Association, San Francisco, June 24, 1958.

U. S. Public Health Service Postdoctoral Research Fellow in Arthritis and Metabolic Diseases (Dr. Lillehei). The John and Mary R. Markle Scholar in the Medical Sciences (Dr. MacLean).

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