Singh Phani Bhushan, Tiwary Pushpakant, Singh Sanjeev K, Pandey Ratna, Roy Atanu, Kar Amrita Ghosh, Basu Somprakas, Tiwari Anil Kumar
Senior Resident, Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India.
Colonel, Department of Radiodiagnosis, Military Hospital, Bareilly, Uttar Pradesh, India.
J Clin Diagn Res. 2017 Jun;11(6):CC25-CC30. doi: 10.7860/JCDR/2017/28804.10124. Epub 2017 Jun 1.
Appendicitis poses a great health problem worldwide. Previous studies demonstrated structural damage to neuronal network and interstitial cell of Cajal in appendicitis. Above observations suggest for the alterations in appendicular motility/contractility in appendicitis. But the mechanisms involved in mediating the contractility in inflamed vermiform appendix is not known till date.
The present in vitro study was performed to find out the mechanisms responsible for contractility in the inflamed human vermiform appendix.
Contractions of the longitudinal muscle strips of inflamed appendix were recorded in vitro at 37±0.5°C. Control contractions were recorded for 30 min after an initial tension of 0.5 gram. Initially dose-response experiments of agonists (acetylcholine, serotonin and histamine) were performed separately and the dose that produced maximum contraction was determined with each agonist. This maximal dose of agonist was used to elicit contractions in next series of experiments before and after pre-treatment with appropriate antagonists like atropine, ondansetron (5-HT antagonist) and chlorpheniramine maleate respectively.
Acetylcholine (ACh) and serotonin (5-HT) elicited maximum amplitude of contraction at 10 µM and 1 µM concentration respectively. These contractions were significantly blocked by prior exposure of muscle strips with atropine (100 µM) and ondansetron (10 µM). Histamine produced very low amplitude of contractions in comparison to ACh or 5-HT and did not exhibit dose-response relations. The histamine induced contractions were blocked by H antagonist chlorpheniramine maleate (100 µM).
The observations suggested that the contractility of longitudinal muscle strips of inflamed vermiform appendix in human beings was predominantly mediated by muscarinic and serotonergic (5-HT) mechanisms, whereas, histaminergic mechanisms played a minor role in mediating the contractility.
阑尾炎在全球范围内构成了一个重大的健康问题。先前的研究表明，阑尾炎患者的神经网络和 Cajal 间质细胞存在结构损伤。上述观察结果提示阑尾炎患者阑尾的运动性/收缩性发生了改变。但迄今为止，尚不清楚介导发炎阑尾收缩性的机制。
进行本体外研究以找出导致发炎的人类阑尾收缩的机制。
在 37±0.5°C 下体外记录发炎阑尾纵行肌条的收缩情况。在初始张力为 0.5 克后记录 30 分钟的对照收缩情况。首先分别进行激动剂（乙酰胆碱、血清素和组胺）的剂量反应实验，并确定每种激动剂产生最大收缩的剂量。在接下来的一系列实验中，分别用阿托品、昂丹司琼（5 - HT 拮抗剂）和马来酸氯苯那敏等适当拮抗剂预处理前后，使用该激动剂的最大剂量引发收缩。
乙酰胆碱（ACh）和血清素（5 - HT）分别在 10 µM 和 1 µM 浓度下引发最大收缩幅度。预先用阿托品（100 µM）和昂丹司琼（10 µM）处理肌条后，这些收缩明显受到抑制。与 ACh 或 5 - HT 相比，组胺产生的收缩幅度非常低，且未表现出剂量反应关系。组胺诱导的收缩被 H 拮抗剂马来酸氯苯那敏（100 µM）阻断。
这些观察结果表明，人类发炎阑尾纵行肌条的收缩性主要由毒蕈碱能和血清素能（5 - HT）机制介导，而组胺能机制在介导收缩性方面起次要作用。
