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Beneficial effect of preconditioning on ischemia-reperfusion injury in the rat bladder in vivo

机译：预处理对大鼠体内缺血再灌注损伤的有益作用

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We investigated the effect of preconditioning on ischemia-reperfusion injury in the rat bladder. Rat abdominal aorta was clamped with a small clip to induce ischernia-reperfusion injury in the bladder. Twelve-week-old male SD rats were divided into three groups; sham-operated control (Cont), 30 min ischemia-60 min reperfusion (IR) and three times of 5 min ischemia and then 30 min ischemia-60 min reperfusion (PC) groups. The bladder functions were estimated by cystometric and functional studies. Contractile response curves to increasing concentrations of carbachol were constructed in the absence and presence of various concentrations of subtype selective muscarinic antagonists, i.e. atropine (non-selective), pirenzepine (M1 selective), methoctramine (M2 selective), and 4-DANIP (M1/M3 selective). We also measured tissue levels of malonaldehyde (NIDA) and examined possible histological changes in these rats' bladders. Preconditioning partially prevented the reduction of bladder dysfunction induced by ischernia-reperfusion. Estimation of the pA2 values for atropine, pirenzepine, methoctramine, and 4-DAMP indicates that the carbachol-induced contractile response in bladder dome is mediated through the M3 receptor subtype in all groups. The NIDA concentration in the IR group was significantly larger than that of the control group, and preconditioning significantly reduced NIDA production in the bladder. In histological studies, the ischemia-reperfusion with or without preconditioning caused infiltration of leukocytes and rupture of microcirculation in the regions of submucosa and smooth muscle without a corresponding sloughing of mucosal cells. Our data indicate that preconditioning has a beneficial effect on ischemia-reperfusion injury in the rat bladder. (c) 2007 Elsevier Inc. All rights reserved.
机译：我们研究了预处理对大鼠膀胱缺血-再灌注损伤的影响。用小夹子夹住大鼠腹主动脉，以诱导膀胱缺血再灌注损伤。十二周大的雄性SD大鼠分为三组。假手术对照组（续），缺血30分钟-再灌注60分钟（IR）和缺血5分钟再灌注3次，缺血30分钟-再灌注60分钟（PC）组。膀胱功能通过膀胱测量和功能研究进行评估。在不存在和存在各种浓度的亚型选择性毒蕈碱拮抗剂（即阿托品（非选择性），哌仑西平（M1选择性），甲辛达明（M2选择性）和4-DANIP（M1）的情况下，构建了对浓度不断升高的卡巴胆碱的收缩反应曲线。 / M3选择性）。我们还测量了丙二醛（NIDA）的组织水平，并检查了这些大鼠膀胱中可能的组织学变化。预处理部分地防止了由缺血再灌注引起的膀胱功能障碍的减轻。阿托品，哌仑西平，甲氧明和4-DAMP的pA2值的估算表明，在所有组中，卡巴胆碱引起的膀胱穹顶收缩反应均通过M3受体亚型介导。 IR组的NIDA浓度显着高于对照组，而预处理显着降低了膀胱中NIDA的产生。在组织学研究中，有或没有预处理的局部缺血-再灌注引起粘膜下层和平滑肌区域白细胞浸润和微循环破裂，而没有相应的粘膜细胞脱落。我们的数据表明，预处理对大鼠膀胱缺血-再灌注损伤具有有益的作用。 （c）2007 Elsevier Inc.保留所有权利。

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