icatibant and Peritonitis

This work investigated the role of bradykinin in viscerosensitivity before and during inflammation in two models of visceral pain induced by rectal distension (RD) or "abdominal distension" (AD) in rats. RD induced both inhibition of colonic motility and an increase of abdominal spike bursts. Bradykinin receptor antagonist, Hoe 140 did not affect any of the RD-induced responses. After TNB-induced rectal inflammation, colonic inhibition and the number of abdominal contractions were enhanced. Hoe 140 selectively reduced the abdominal response to the highest distension volume, without affecting the colonic response. In AD group, acetic acid inhibited gastric emptying and increased the number of abdominal contractions, whereas the same volume of saline did not affect any of the responses. Before inflammation, Hoe 140 (1-5 mg/kg, intraperitoneally) did not affect per se abdominal and gastric emptying responses; in contrast, at 5 mg/kg, intraperitoneally, it reduced significantly (P < 0.05) both acetic acid-induced responses. We conclude that bradykinin is involved in viscerosensitivity changes related to abdominal and rectal distension in inflammatory conditions.

Topics: Abdominal Pain; Acetates; Acetic Acid; Animals; Bradykinin; Bradykinin Receptor Antagonists; Colon; Gastrointestinal Motility; Male; Peritonitis; Proctitis; Rats; Rats, Wistar; Receptors, Bradykinin; Trinitrobenzenesulfonic Acid