Effect of atenolol pre-treatment in heart damage in a model of intestinal ischemia-reperfusion

Abstract Purpose: To investigate the effects of atenolol in inflammatory mediator and oxidative stress in a myocardial injury by intestinal ischemia/reperfusion in rat model. Methods: Adult Wistar male rats were randomly (n=8), anesthetized and divided in: Sham: submitted to operation only; group SS+IR: intravenous saline infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); group AT+IR: intravenous atenolol infusion (2 mg/kg) following superior mesenteric artery occlusion during 60 minutes (ischemia) and open for 120 minutes (reperfusion); and group AT+I+AT+R: intravenous atenolol infusion following superior mesenteric artery occlusion during 60 minutes (ischemia) and in the time 45 minutes other atenolol doses were administrated and the artery was open for 120 minutes (reperfusion), all animals were submitted to muscular relaxation for mechanical ventilation. In the end of experiment the animals were euthanized and the hearts tissue were morphology analyzed by histology and malondialdehyde by ELISA, and the plasma were analyzed for tumor necrosis factor-alpha by ELISA. Results: The group SS+IR demonstrated the higher malondialdehyde levels when compared with the atenolol treated-groups (p=0.001) in the heart tissue. The tumor necrosis factor-alpha level in plasma decrease in the treated groups when compared with SS+IR group (p=0.001). Histology analyses demonstrate pyknosis, edema, cellular vacuolization, presence of inflammatory infiltrate and band contraction in the heart tissue of the rats. Conclusion: Atenolol significantly reduce the degree of cardiac damage after intestinal ischemia-reperfusion.

摘要
**目的**：探讨阿替洛尔（atenolol）对肠缺血再灌注（intestinal ischemia/reperfusion）诱导大鼠心肌损伤模型中炎症介质及氧化应激的影响。
**方法**：选取成年雄性Wistar大鼠，按随机原则分为4组，每组8只，麻醉后行如下处理：假手术组（Sham组）：仅行手术操作；SS+IR组：经静脉输注生理盐水，于肠系膜上动脉（superior mesenteric artery）阻断60分钟（缺血）后开放血管，再灌注120分钟；AT+IR组：经静脉输注阿替洛尔（2 mg/kg），于肠系膜上动脉阻断60分钟（缺血）后开放血管，再灌注120分钟；AT+I+AT+R组：肠系膜上动脉阻断60分钟（缺血）时经静脉输注阿替洛尔，且于缺血45分钟时追加阿替洛尔剂量，随后开放动脉再灌注120分钟。所有大鼠均予肌肉松弛并行机械通气。实验结束后处死大鼠，取心肌组织行组织形态学分析，采用酶联免疫吸附试验（ELISA）检测心肌组织中丙二醛（malondialdehyde）水平；采集血浆采用ELISA检测肿瘤坏死因子-α（tumor necrosis factor-alpha）水平。
**结果**：与阿替洛尔干预组相比，SS+IR组心肌组织中的丙二醛水平显著升高（p=0.001）。与SS+IR组相比，干预组血浆肿瘤坏死因子-α水平显著降低（p=0.001）。组织学分析显示，大鼠心肌组织可见核固缩、水肿、细胞空泡变性、炎性浸润及肌带收缩。
**结论**：阿替洛尔可显著减轻肠缺血再灌注后心肌损伤程度。