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首页> 外文期刊>Naunyn-Schmiedeberg's Archives of Pharmacology >Captopril improves postresuscitation hemodynamics protective against pulmonary embolism by activating the ACE2/Ang-(1-7)/Mas axis
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Captopril improves postresuscitation hemodynamics protective against pulmonary embolism by activating the ACE2/Ang-(1-7)/Mas axis

机译：卡托普利可通过激活ACE2 / Ang-（1-7）/ Mas轴改善复苏后的血流动力学，从而预防肺栓塞

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摘要

Acute pulmonary embolism (APE) has a very high mortality rate, especially at cardiac arrest and even after the return of spontaneous circulation (ROSC). This study investigated the protective effect of the angiotensin-converting enzyme (ACE) inhibitor captopril on postresuscitation hemodynamics, in a porcine model of cardiac arrest established by APE. Twenty-nine Beijing Landrace pigs were infused with an autologous thrombus leading to cardiac arrest and subjected to standard cardiopulmonary resuscitation and thrombolysis. Ten resuscitated pigs were randomly and equally apportioned to receive either captopril (22.22 mg/kg) infusion or the same volume saline, 30 min after ROSC. Hemodynamic changes and ACE-Ang II-angiotensin II type 1 receptor (AT1R) and ACE2/Ang-(1-7)/Mas receptor axis levels were determined. APE was associated with a decline in mean arterial pressure and a dramatic increase in pulmonary artery pressure and mean right ventricular pressure. After ROSC, captopril infusion was associated with significantly lower mean right ventricular pressure and systemic and pulmonary vascular resistance, faster heart rate, and higher Ang-(1-7) levels, ACE2/ACE, and Ang-(1-7)/Ang II, compared with the saline infusion. The ACE2/Ang-(1-7)/Mas pathway correlated negatively with external vascular lung water and pulmonary vascular permeability and positively with the right cardiac index. In conclusion, in a pig model of APE leading to cardiac arrest, captopril infusion was associated with less mean right ventricular pressure overload after resuscitation, compared with saline infusion. The reduction in systemic and pulmonary vascular resistance associated with captopril may be by inhibiting the ACE-Ang II-AT1R axis and activating the ACE2/Ang-(1-7)/Mas axis.
机译：急性肺栓塞（APE）的死亡率很高，尤其是在心脏骤停甚至自发循环（ROSC）恢复后。这项研究调查了血管紧张素转换酶（ACE）抑制剂卡托普利对复苏后血流动力学的保护作用，这是由APE建立的猪心脏骤停模型。向29只北京长白猪注入自体血栓，导致心脏骤停，并进行标准的心肺复苏和溶栓治疗。在ROSC后30分钟，随机对10只复苏的猪进行均等分配以接受卡托普利（22.22 mg / kg）输注或等体积的盐水。测定血流动力学变化和ACE-Ang II-血管紧张素II 1型受体（AT1R）和ACE2 / Ang-（1-7）/ Mas受体轴水平。 APE与平均动脉压下降以及肺动脉压和平均右心室压显着增加有关。 ROSC后，卡托普利输注与显着降低平均右心室压力和全身和肺血管阻力，更快的心率以及更高的Ang-（1-7）水平，ACE2 / ACE和Ang-（1-7）/ Ang相关二，与生理盐水相比输注。 ACE2 / Ang-（1-7）/ Mas途径与外部血管肺水和肺血管通透性呈负相关，与正确的心脏指数呈正相关。总之，在APE导致心脏骤停的猪模型中，与盐水灌注相比，卡托普利灌注与复苏后平均右心室压力超负荷较少相关。与卡托普利有关的全身和肺血管阻力的降低可能是通过抑制ACE-Ang II-AT1R轴并激活ACE2 / Ang-（1-7）/ Mas轴。

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