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Philip W. Wright, MD; Bernard Goodhead, ChM

AMA Arch Surg. 1970;100(1):42-46.

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

It has been substantiated that vascular phenomena are important in the pathogenesis of acute hemorrhagic pancreatitis.^1-3 Impairment of pancreatic blood has been stressed as an important event in the progression of edematous to hemorrhagic pancreatitis; and there is evidence that the extent and the severity of the disease and, in particular, the progression to hemorrhagic necrosis is determined by the development of stasis or thrombosis within the pancreatic microcirculation.³ It has been suggested that impairment of local blood flow in the gland retards the absorption of proteolytic enzymes into the circulation, thereby increasing the susceptibility of the pancreas to further injury by enzymes and toxic products retained in the gland.¹

Attempts to modify the course of this disease have seldom taken these factors into account; and it is postulated that if a satisfactory blood flow could be maintained, enzymes and their digestive products would continue to be . . . [Full Text PDF of this Article]

Author Affiliations
Torrance, Calif

From the Department of Surgery, Harbor General Hospital, Torrance, Calif. and the University of California School of Medicine, Los Angeles. During the study, Dr. Goodhead was a research fellow of the Long Beach Heart Association and worked under the directionship of Dr. M. J. Orloff, Harbor General Hospital, and is presently at the University of Texas, Medical School at San Antonio, San Antonio. Dr. Wright is presently in Long Beach, Calif.

Footnotes
Submitted for publication May 16, 1969.

Reprint requests to Department of Surgery, University of Texas, Medical School at San Antonio, 7703 Floyd Curl Dr, San Antonio, Tex 78229 (Dr. Goodhead).

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