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首页> 外文期刊>Cytokine >Effects of captopril and angiotensin II receptor blockers (AT1, AT2) on myocardial ischemia-reperfusion induced infarct size.
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Effects of captopril and angiotensin II receptor blockers (AT1, AT2) on myocardial ischemia-reperfusion induced infarct size.

机译:卡托普利和血管紧张素II受体阻滞剂(AT1,AT2)对心肌缺血再灌注引起的梗塞面积的影响。

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The renin-angiotensin system (RAS) plays a major role in regulating the cardiovascular system, and disorders of the RAS contribute largely to the cardiac pathophysiology, including myocardial ischemia-reperfusion (MI/R) injury. Two subtypes of angiotensin II (Ang II) receptors have been defined on the basis of their differential pharmacological properties. The current study was undertaken to address the question as to whether the inhibition of the angiotensin converting enzyme (ACE) by captopril and the AT1 and AT2 receptor blockers losartan and PD123319 modulate MI/R-induced infarct size in an in vivo rat model. To produce necrosis, a branch of the descending left coronary artery was occluded for 30 min followed by two hours of reperfusion. ECG changes, blood pressure, and heart rate were measured during the experiment. Captopril (3 mg/kg), losartan (2 mg/kg), and PD123319 (20 mug/kg/min) were given in an IV 10 min before ischemia and were continued during the ischemic period. The infarcted area was measured by TTC staining. The volume of infarct and the risk zone was determined by planimetry. Compared to the control group (55.62+/-4.00%) both captopril and losartan significantly reduced the myocardial infarct size (30.50+/-3.26% and 37.75+/-4.44%), whereas neither PD123319 nor PD123319+losartan affected the infarct size volume (46.50+/-3.72% and 54.62+/-2.43%). Our data indicates that captopril and losartan exert cardioprotective activity after an MI/R injury. Also, infarct size reduction by losartan was halted by a blockade of the AT2 receptor. Therefore, the activation of AT2 receptors may be potentially protective and appear to oppose the effects mediated by the AT1 receptors.
机译:肾素-血管紧张素系统(RAS)在调节心血管系统中起主要作用,并且RAS疾病在很大程度上有助于心脏病理生理,包括心肌缺血再灌注(MI / R)损伤。根据其不同的药理特性,已定义了血管紧张素II(Ang II)受体的两种亚型。进行当前的研究以解决关于卡托普利和AT1和AT2受体阻滞剂氯沙坦和PD123319对血管紧张素转化酶(ACE)的抑制是否在体内大鼠模型中调节MI / R诱导的梗塞大小的问题。为了产生坏死,将左冠状动脉下降分支闭塞30分钟,然后再灌注两个小时。实验期间测量心电图变化,血压和心率。在缺血前10分钟的静脉输注卡托普利(3 mg / kg),氯沙坦(2 mg / kg)和PD123319(20杯/ kg / min),并在缺血期间继续服用。通过TTC染色测量梗塞面积。梗死面积和危险区通过平面测量法确定。与对照组相比(55.62 +/- 4.00%)卡托普利和氯沙坦均显着降低了心肌梗死面积(30.50 +/- 3.26%和37.75 +/- 4.44%),而PD123319和PD123319 +氯沙坦均未影响心肌梗死面积体积(46.50 +/- 3.72%和54.62 +/- 2.43%)。我们的数据表明卡托普利和氯沙坦在MI / R损伤后发挥心脏保护作用。同样,氯沙坦对梗死面积的缩小也被AT2受体的阻断所阻止。因此,AT2受体的激活可能具有潜在的保护作用,并且似乎与AT1受体介导的作用相反。

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