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JAMES W. RYAN, MD; JOHN G. MOFFAT, MD; ALAN G. THOMPSON, MD, FRCS

AMA Arch Surg. 1965;91(1):14-24.

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

INVESTIGATIONS defining the actions and properties of bradykinin have provided a basis for the hypothesis that bradykinin, and/or a congener, is a humoral mediator of the inflammatory response. The ability of bradykinin to cause pain,² vasodilatation,²⁴ increased vascular permeability,¹⁰ hypotension,³³ smooth muscle stimulation,³³ and leucocyte accumulation,^10,28 has led to a consideration of a possible role of this polypeptide in a disease process, such as acute hemorrhagic pancreatitis, characterized by manifestations of these actions.³⁸ A hypothesis linking bradykinin to the early pathogenesis of acute pancreatitis is even more attractive when one considers that the pancreas contains ample stores of trypsinogen and kallikreinogen, each of which in active form releases active bradykinin and functionally related polypeptides.¹⁵ Furthermore, the substrate for bradykinin release, bradykininogen, is a normal pseudoglobin of plasma, lymph, and interstitial fluid and as such is continuously available to the pancreas.³³

Hilton and . . . [Full Text PDF of this Article]

Author Affiliations
BETHESDA, MD; MONTREAL

From McGill University Surgical Clinic, Montreal General Hospital.

Footnotes
Read before 22nd Annual Meeting, Central Surgical Association, Milwaukee, March 4-6, 1965.

Reprint requests to National Institutes of Health, Bldg 10, Room 4S-223, Bethesda 14, Md (Dr. Ryan).

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