CAJ | 학술논문

目的研究P2X1受体在滥用氯胺酮导致膀胱功能障碍患者膀胱组织中的表达及其临床意义.讨论P2X1受体在滥用氯胺酮引起膀胱功能障碍中的作用.方法采用免疫组织化学方法分别检测36例滥用氯胺酮引起膀胱功能障碍患者(实验组)和36例正常膀胱组织(对照组)中P2X1受体、M2受体、M3受体的表达情况,利用全自动显微镜及图像分析系统对免疫组化染色结果进行图像采集分析、测量其平均灰度值,同时比较两组间P2X1受体、M2受体、M3受体表达的差异.结果 P2X1受体主要在膀胱黏膜移行上皮细胞表达,实验组P2X1受体表达明显增强,与对照组比较差异有统计学意义(P＜0.01),而M2受体、M3受体表达与对照组比较无明显差异(P＞0.01).结论滥用氯胺酮引起膀胱功能障碍患者膀胱组织中P2X1受体表达显著增强,而M2受体、M3受体并未异常表达,提示P2X1受体上调可能在滥用氯胺酮导致膀胱过度活动中发挥关键作用.
목적 연구P2X1수체재람용록알동도치방광공능장애환자방광조직중적표체급기림상의의.토론P2X1수체재람용록알동인기방광공능장애중적작용.방법 채용면역조직화학방법분별검측36례람용록알동인기방광공능장애환자(실험조)화36례정상방광조직(대조조)중P2X1수체、M2수체、M3수체적표체정황,이용전자동현미경급도상분석계통대면역조화염색결과진행도상채집분석、측량기평균회도치,동시비교량조간P2X1수체、M2수체、M3수체표체적차이.결과 P2X1수체주요재방광점막이행상피세포표체,실험조P2X1수체표체명현증강,여대조조비교차이유통계학의의(P＜0.01),이M2수체、M3수체표체여대조조비교무명현차이(P＞0.01).결론 람용록알동인기방광공능장애환자방광조직중P2X1수체표체현저증강,이M2수체、M3수체병미이상표체,제시P2X1수체상조가능재람용록알동도치방광과도활동중발휘관건작용.
Objectives To evaluate the expression of P2X1 receptor in ketamine induced bladder dysfunction,and discus its clinical significance.Methods The expression of P2X1,M1 and M2 receptor in 36 cases of normal bladder and 36 cases of ketamine induced bladder dysfunction was detected by Immunohistochemistry SABC assay.The image was acquired by automatic microscope and the mean gray level value was analyzed by computer image analysis system.Results P2X1 receptor was mainly expressed in transitional epithelium of the bladder.The expression of P2X1 receptor was low in the normal group,which was significantly increased in the case group.The level of the expression of P2X1 receptor was statically significant(P ＜0.01).However,the level of expression of M1 and M2 receptor was no statically significant(P ＞0.01) in comparison with the two groups.Conclusions The expression of P2X1 receptor was significantly increased in the bladder tissue of the patient with abuse of katamine induced bladder dysfunction.And there was no difference of the expression of M1 and M2 receptor between the control and ketamine groups.These data indicated that the P2X1 receptor up-regulation may underlie detrusor overactivity in cases of ketamine induced bladder dysfunction.