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Captopril improves postresuscitation hemodynamics protective against pulmonary embolism by activating the ACE2/Ang-(1-7)/Mas axis.
Naunyn Schmiedebergs Arch Pharmacol. 2016 Nov; 389(11):1159-1169.NS

Abstract

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.

Authors+Show Affiliations

Department of Emergency Medicine, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Workers Stadium Road No. 8, Chaoyang District, 100020, Beijing, China.Department of Emergency Medicine, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Workers Stadium Road No. 8, Chaoyang District, 100020, Beijing, China. lcscyyy@163.com.Department of Emergency Medicine, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Workers Stadium Road No. 8, Chaoyang District, 100020, Beijing, China.Department of Emergency Medicine, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Workers Stadium Road No. 8, Chaoyang District, 100020, Beijing, China.Department of Emergency Medicine, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Workers Stadium Road No. 8, Chaoyang District, 100020, Beijing, China.Department of Emergency Medicine, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Workers Stadium Road No. 8, Chaoyang District, 100020, Beijing, China.Department of Radiology, Beijing Chaoyang Hospital, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Capital Medical University, Beijing, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27449068

Citation

Xiao, Hong-Li, et al. "Captopril Improves Postresuscitation Hemodynamics Protective Against Pulmonary Embolism By Activating the ACE2/Ang-(1-7)/Mas Axis." Naunyn-Schmiedeberg's Archives of Pharmacology, vol. 389, no. 11, 2016, pp. 1159-1169.
Xiao HL, Li CS, Zhao LX, et al. Captopril improves postresuscitation hemodynamics protective against pulmonary embolism by activating the ACE2/Ang-(1-7)/Mas axis. Naunyn Schmiedebergs Arch Pharmacol. 2016;389(11):1159-1169.
Xiao, H. L., Li, C. S., Zhao, L. X., Yang, J., Tong, N., An, L., & Liu, Q. T. (2016). Captopril improves postresuscitation hemodynamics protective against pulmonary embolism by activating the ACE2/Ang-(1-7)/Mas axis. Naunyn-Schmiedeberg's Archives of Pharmacology, 389(11), 1159-1169.
Xiao HL, et al. Captopril Improves Postresuscitation Hemodynamics Protective Against Pulmonary Embolism By Activating the ACE2/Ang-(1-7)/Mas Axis. Naunyn Schmiedebergs Arch Pharmacol. 2016;389(11):1159-1169. PubMed PMID: 27449068.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Captopril improves postresuscitation hemodynamics protective against pulmonary embolism by activating the ACE2/Ang-(1-7)/Mas axis. AU - Xiao,Hong-Li, AU - Li,Chun-Sheng, AU - Zhao,Lian-Xing, AU - Yang,Jun, AU - Tong,Nan, AU - An,Le, AU - Liu,Qi-Tong, Y1 - 2016/07/22/ PY - 2016/06/09/received PY - 2016/07/14/accepted PY - 2016/7/28/pubmed PY - 2017/2/22/medline PY - 2016/7/25/entrez KW - ACE2/Ang-(1-7)-Mas axis KW - Acute pulmonary embolism KW - Captopril KW - Cardiac arrest KW - Restoring spontaneous circulation SP - 1159 EP - 1169 JF - Naunyn-Schmiedeberg's archives of pharmacology JO - Naunyn Schmiedebergs Arch Pharmacol VL - 389 IS - 11 N2 - 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. SN - 1432-1912 UR - https://www.unboundmedicine.com/medline/citation/27449068/Captopril_improves_postresuscitation_hemodynamics_protective_against_pulmonary_embolism_by_activating_the_ACE2/Ang__1_7_/Mas_axis_ L2 - https://dx.doi.org/10.1007/s00210-016-1278-7 DB - PRIME DP - Unbound Medicine ER -