Masick J M, Levin R M, Hass M A
Division of Basic and Pharmaceutical Sciences, Albany College of Pharmacy, NY 12208, USA.
Prostaglandins Other Lipid Mediat. 2001 Oct;66(3):211-9. doi: 10.1016/s0090-6980(01)00151-4.
Partial outlet obstruction of the urinary bladder has been demonstrated to induce specific dysfunctions in cellular and sub-cellular membrane structures within the bladder's smooth muscle and mucosal compartments. Recent studies have linked these membrane dysfunctions to alterations in phospholipid metabolism leading to mobilization of free arachidonic acid, the precursor for synthesis of prostaglandins (PG). The purpose of this study was to determine if partial outlet obstruction of the urinary bladder induces changes in the capacity of bladder smooth muscle and mucosa to generate PG. PG were isolated from control and partially obstructed urinary bladder smooth muscle and mucosa of male New Zealand White (NZW) rabbits. PG concentrations (PGE2, PGF2alpha and PGI2, as its stable metabolite 6-keto-PGF1alpha) were determined after 30 minute incubations using enzyme-linked immunoassay (ELISA) kits. In both control and obstructed rabbit urinary bladders, PG generation was significantly higher in isolated mucosa than muscle tissues. A significantly higher concentration of PGF2alpha, and 6-keto-PGF1alpha was measured in obstructed muscle tissue relative to controls. The concentration of 6-keto-PGF1alpha was also significantly higher than the concentrations measured for PGE2 and PGF2alpha in both control and obstructed smooth muscle samples. The generation of PGE2 was significantly higher in rabbit urinary bladder mucosa than either PGF2alpha or 6-keto-PGF1alpha in both control and obstructed samples. The capacity of obstructed mucosal tissue to generate 6-keto-PGF1alpha was significantly higher than control tissue, while no significant differences in PGE or PGF2alpha generation were noted. These data suggest obstruction of the urinary bladder induce specific elevations in PG in both smooth muscle and mucosal tissues.
膀胱部分出口梗阻已被证明会在膀胱平滑肌和黏膜区域的细胞及亚细胞膜结构中引发特定功能障碍。近期研究已将这些膜功能障碍与磷脂代谢改变联系起来，磷脂代谢改变会导致游离花生四烯酸的动员，花生四烯酸是前列腺素（PG）合成的前体。本研究的目的是确定膀胱部分出口梗阻是否会引起膀胱平滑肌和黏膜生成PG的能力发生变化。从雄性新西兰白兔（NZW）的对照膀胱和部分梗阻膀胱的平滑肌及黏膜中分离出PG。使用酶联免疫吸附测定（ELISA）试剂盒在孵育30分钟后测定PG浓度（PGE2、PGF2α和PGI2，以其稳定代谢产物6-酮-PGF1α表示）。在对照和梗阻的兔膀胱中，分离出的黏膜中PG生成均显著高于肌肉组织。与对照组相比，梗阻肌肉组织中PGF2α和6-酮-PGF1α的浓度显著更高。在对照和梗阻的平滑肌样本中，6-酮-PGF1α的浓度也显著高于PGE2和PGF2α的浓度。在对照和梗阻样本中，兔膀胱黏膜中PGE2的生成均显著高于PGF2α或6-酮-PGF1α。梗阻黏膜组织生成6-酮-PGF1α的能力显著高于对照组织，而PGE或PGF2α生成未发现显著差异。这些数据表明膀胱梗阻会导致平滑肌和黏膜组织中PG特异性升高。
