变更urothelial-mediated缺血性膀胱的基调:类花生酸的作用。

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Azadzoi公里,海姆VK、Tarcan T Siroky MB

变更urothelial-mediated缺血性膀胱的基调:类花生酸的作用。

Neurourol Urodyn。2004; 23 (3): 258 - 64。

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15098224 (在PubMed

]

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目的:以前我们发现缺血改变膀胱平滑肌收缩性的兔子。本研究主要探讨膀胱上皮的作用和eicosanoid-release缺血性膀胱平滑肌不稳定。材料与方法:雄性新西兰白兔分为治疗(n = 12)和年龄控制(n = 10)组。治疗组接受气球髂动脉内皮损伤,然后收到了4周的胆固醇饮食,其次是4周的常规饮食。对照组接受常规饮食为8周。8周后,髂动脉的血液流动和膀胱以及膀胱氧张力都被记录下来。在一半的每个缺血性和控制膀胱,尿道上皮被移除。膀胱组织器官浴处理和酶免疫分析法(EIA)的前列腺素(后卫)和白细胞三烯(LTs)。结果:髂动脉的血流量明显下降,膀胱壁血流,和膀胱氧张力被发现治疗组。膀胱缺血增加的频率和振幅基线自发的平滑肌收缩性。 Ischemic tissues with urothelium (Uro+) demonstrated significant increases in the contractile response to electrical field stimulation (EFS) and carbachol relative to control Uro+ tissues. Urothelial removal increased smooth muscle contraction in the control tissues but had no significant effect in the ischemic/hypoxic tissues. Contraction of control tissues without urothelium (Uro-) was similar to contraction of ischemic Uro+ tissues. Contractions of ischemic Uro+ and control Uro- tissues were unchanged after treatment with the cyclooxygenase (COX) inhibitor indomethacin, while they were significantly reduced by the 5-lipoxygenase (5-LO) inhibitor NDGA. EIA showed no change in PGs release from the ischemic urothelium, but significant increase in PGF(2-alpha) and thromboxane A(2) release from the ischemic suburothelial tissue. Ischemia increased the release of LTB(4), LTC(4), and LTE(4) from both urothelium and suburothelial tissue. CONCLUSIONS: Our studies suggest loss of urothelial-mediated tone and LTs-mediated smooth muscle instability in the chronically ischemic/hypoxic bladder.

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药物靶点

药物	目标	类	生物	药理作用	行动
Masoprocol	花生四烯酸5-lipoxygenase	蛋白质	人类	是的	抑制剂	细节