Julia V, Mezzasalma T, Buéno L
Department of Pharmacology, INRA, Toulouse, France.
Dig Dis Sci. 1995 Sep;40(9):1913-21. doi: 10.1007/BF02208656.
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.
本研究在大鼠直肠扩张（RD）或“腹部扩张”（AD）诱导的两种内脏痛模型中，调查了缓激肽在炎症发生前和炎症期间内脏敏感性中的作用。RD诱导结肠运动抑制和腹部峰电位爆发增加。缓激肽受体拮抗剂Hoe 140对RD诱导的任何反应均无影响。在三硝基苯磺酸（TNB）诱导直肠炎症后，结肠抑制和腹部收缩次数增强。Hoe 140选择性降低了对最大扩张体积的腹部反应，而不影响结肠反应。在AD组中，乙酸抑制胃排空并增加腹部收缩次数，而相同体积的生理盐水对任何反应均无影响。在炎症发生前，腹腔注射1-5mg/kg的Hoe 140本身不影响腹部和胃排空反应；相反，腹腔注射5mg/kg时，它显著降低（P<0.05）乙酸诱导的两种反应。我们得出结论，缓激肽参与了炎症状态下与腹部和直肠扩张相关的内脏敏感性变化。
