Kaya Tijen Temiz, Koyluoglu Gokhan, Karadas Baris, Yildiz Turan, Bagcivan Ihsan, Ceran Canan, Gökgöz Sehsuvar
Department of Pharmacology, Faculty of Medicine, Cumhuriyet University, 58030 Sivas, Turkey.
J Surg Res. 2004 Aug;120(2):219-24. doi: 10.1016/j.jss.2003.12.010.
The mechanisms involved in the impaired gallbladder contractile response in peritonitis are unknown. The aim of this study was to determine the effect of peritonitis on the contraction and relaxation responses to different agonists in gallbladder smooth muscle in guinea pig.
Peritonitis was induced by cecal ligation and puncture (CLP) in 10 guinea pigs. Another group of 10 guinea pigs underwent a sham operation and acted as controls. Twenty-four hours after the operation, the guinea pigs were killed, and gallbladder strips were placed in organ bath. The contraction responses to KCl, carbachol, and histamine, and relaxation responses to cyclooxygenase inhibitors (indomethacin, nimesulide, and DFU) on KCl-induced contractions were recorded.
There was no significant difference between the contractile responsiveness to KCl, but maximum contractile responses (E(max)) to carbachol and histamine were significantly reduced. Indomethacin, nimesulide, and DFU concentration dependently inhibited on KCl-induced contractions of gallbladder smooth muscle. E(max) values of indomethacin, nimesulide, and DFU were significantly reduced in the peritonitis group compared with controls (P < 0.05). The inhibitor effects of nimesulide and DFU were considerably similar, but inhibitor effect of indomethacin was significantly less than that measured for nimesulide and DFU in both control and peritonitis groups (P < 0.05).
The contraction responses to carbachol and histamine and relaxation responses to COX inhibitors on gallbladder smooth muscle are significantly decreased by peritonitis. Although the mechanism of the decrease in contraction and relaxation responses in CLP-induced peritonitis is completely unknown, we speculate that impaired smooth muscle responses may be related to an alteration in the regulation of receptor/postreceptor excitation-response coupling and/or through changes on Ca(2+) influx.
腹膜炎时胆囊收缩反应受损的机制尚不清楚。本研究旨在确定腹膜炎对豚鼠胆囊平滑肌对不同激动剂的收缩和舒张反应的影响。
对10只豚鼠行盲肠结扎穿刺术（CLP）诱导腹膜炎。另一组10只豚鼠行假手术作为对照。术后24小时处死豚鼠，将胆囊条置于器官浴槽中。记录对氯化钾、卡巴胆碱和组胺的收缩反应，以及对环氧化酶抑制剂（吲哚美辛、尼美舒利和DFU）对氯化钾诱导收缩的舒张反应。
对氯化钾的收缩反应性无显著差异，但对卡巴胆碱和组胺的最大收缩反应（E(max)）显著降低。吲哚美辛、尼美舒利和DFU浓度依赖性抑制胆囊平滑肌氯化钾诱导的收缩。与对照组相比，腹膜炎组吲哚美辛、尼美舒利和DFU的E(max)值显著降低（P < 0.05）。尼美舒利和DFU的抑制作用相当相似，但在对照组和腹膜炎组中，吲哚美辛的抑制作用均显著小于尼美舒利和DFU（P < 0.05）。
腹膜炎可显著降低胆囊平滑肌对卡巴胆碱和组胺的收缩反应以及对COX抑制剂的舒张反应。虽然CLP诱导的腹膜炎中收缩和舒张反应降低的机制完全未知，但我们推测平滑肌反应受损可能与受体/受体后兴奋-反应偶联调节的改变和/或钙内流的变化有关。
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