Intra-pancreatic release of bradykinin during the course experimental pancreatitis in rat

P Jönsson,K Ohlsson

doi:10.1155/s0962935196000282

Abstract

Kallikrein/Kininogn activation is an important pathophysiological event in acute pancreatitis, leading to microcirculatory changes within the gland. Hitherto, only indirect measurements of pancreatic bradykinin formation have been performed, monitoring the peptide in the circulation and in the peritoneal exudate. In the present study, intra-pancreatic bradykinin release was assessed using microdialysis during experimental acute pancreatitis in rat. In mild, oedematous pancreatitis, induced by caerulein hyperstimulation, the levels of bradykinin within the gland were not elevated compared with those of control rats. However, in necrotic pancreatitis, induced by retrograde injection of taurocholate into the pancreatic duct, significantly elevated levels of intraglandular bradykinin were seen. Several rats in this group died whilst in a state of circulatory shock.

Highlights

Release of bradykinin has been demonstrated during acute pancreatitis and is proposed to contribute to the development of hypotension and shock.’[2]
The purpose of this work was to elucidate whether the release of bradykinin in the pancreatic gland is more profuse during taurocholateinduced pancreatitis in rat, often leading to shock, than during caerulein-induced pancreatitis
A severe inflammatory reaction was seen in the pancreatic gland in the taurocholate group with haemorrhage, oedema and necrotic areas, while in the caerulein group, only modest oedema was seen, without bleeding or obvious necrosis

Summary

Introduction

Release of bradykinin has been demonstrated during acute pancreatitis and is proposed to contribute to the development of hypotension and shock.’[2] Bradykinin is one of the most potent vasodilators in man, causing loss of intravascular fluid by increasing the capillary permeability. Direct measurement of activated bradykinin in the circulation is difficult due to the great capacity of blood to both generate and degrade this peptide.7’8 The kinins are rapidly inactivated by carboxypeptidases (kinase I and II) and have an estimated half-life of about 20 s in the human circulation.[9] The plasma levels of bradykinin reported for man vary considerably when measured by bio-assay and radioimmunoassay.[10 11]

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Results

Conclusion