Abstract
THE ability of bradykinin or kallidin to cause hypotension, pain, vasodilatation, increased vascular permeability, smooth muscle stimulation, leucocyte migration, and leucocyte accumulation suggests the possibility that bradykinin may play a part in a disease process, such as acute haemorrhagic pancreatitis, characterized by hypotension, pain, haemoconcentration, dynamic fluid shifts with the accumulation of ascitic fluid, leucocytosis, and œdema and leucocytic infiltration of the gland1,2. The attractiveness of this hypothesis is enhanced by the knowledge that the pancreas contains large quantities of trypsinogen and kallikreinogen, both of which, in active form, are capable of releasing bradykinin from its inactive precursor, bradykininogen. Bradykininogen, as a normal pseudoglobulin of plasma, lymph, and interstitial fluid, is readily available to the pancreas1.
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