Voiding function in mice lacking TRPV 1

目的：有研究报道，瞬时受体电位香草素1(TRPV1)在膀胱炎中起重要作用，即在痛觉过敏和活动亢进中起重要作用。然而，慢性膀胱炎过程中的激活机制还知之甚少。因此，我们评估了缺乏TRPV1(TRPV1 KO)的小鼠在环磷酰胺(CYP)诱导的膀胱炎中的膀胱功能。TRPV1KO组和野生型对照组(WT)分别给予CYP(150 mg/kg)或无菌水。给药45小时后，用七氟醚麻醉小鼠，以便手术插入膀胱内导管。手术结束后，清醒束缚小鼠以恒定速度(0.5ml/小时)注入生理盐水进行膀胱测压。2.组织病理学检查。TRPV1和WT分别给予CYP(150 mg/kg)或赋形剂腹腔注射。管理…后48小时给予更多的环磷酰胺，麻醉小鼠。取完整膀胱，在10%福尔马林缓冲溶液中固定24小时。组织(3微米厚)苏木精-伊红染色。观察组织学损伤，包括出血和炎症反应。结果：1.清醒束缚小鼠的膀胱计数。在给药小鼠中，WT和TRPV1 KO的收缩间期(ICI)无显著差异。西药给药组ICI明显短于给药组。在TRPV1KO中，赋形剂给药组与CYP给药组ICI差异无统计学意义。各组间最大排尿压差异无统计学意义。2.组织病理学检查。给药组小鼠膀胱组织学正常。CYP给药可引起TRPV1KO和WT大鼠膀胱出血和炎症反应。镜下观察，TRPV1组和WT1组小鼠膀胱炎性病变的面积和大小相似。结论：TRPV1可能参与了CYP诱导的小鼠膀胱炎的发病机制。较少

Purpose :Some investivators reported that transient receptor potential vanilloid 1 (TRPV1) played an important role during bladder inflammation, namely in hyperalgesia and hyperactivity. However, the mechanisms of activation during chronic bladder inflammation are poorly understood. Therefore, we evaluated the bladder function in mice lacking TRPV1 (TRPV1 KO) with cyclophosphamide (CYP)-induced cystitis.Methods :1.Cystometryin conscious restrained mice. TRPV1 KO and wild type control (WT) were administered CYP (150 mg/kg) or vehicle (sterile water) intraperitoneally. Forty-five hours after administration of CYP, the mice were anesthetized with sevoflurane for surgical insertion of an intravesical catheter. After the surgery, cystometry was performed in conscious restrained mice by infusing saline into the bladder at a constant rate (0.5 ml/hr).2.Histopathological examination. TRPV1 and WT were administered CYP (150 mg/kg) or vehicle intraperitoneally. Forty-eight hours after administra … More tion of CYP, the mice were anesthetized. Bladder was taken intact and fixed for 24 hours in 10% buffered formalin. Tissue (3 micrometer thickness) was stained with hematoxylin-eosin. Histological damage, including hemorrhage and inflammation were evaluated.Results :1.Cystometry in conscious restrained mice. In vehicle administrated mice, there was no significant difference in intercontraction interval (ICI) between WT and TRPV1 KO. In WT, ICI of CYP administrated group was significantly shorter than that of vehicle administrated group. In TRPV1 KO, there was no significant difference in ICI between vehicle administrated group and CYP administrated group. There was no significant difference in maximal voiding pressure between each group.2.Histopathological examination. Vehicle administrated mice had histologically normal bladders. CYP administration caused hemorrhage and inflammation of bladders in both TRPV1 KO and WT. Under microscopic examination, the area and size of inflammation in the bladder were similar in TRPV1 and WT.Conclusions :TRPV1 might be responsible for mechanisms of bladder hyperactivity in mice with CYP-induced cystitis. Less