Increasing angiotensin-converting enzyme (ACE) 2/ACE axes ratio alleviates early pulmonary vascular remodeling in a porcine model of acute pulmonary embolism with cardiac arrest

Hong-li Xiao, Lian-xing Zhao, Jun Yang, Nan Tong, Le An, Guo-xing Wang, Miao-rong Xie, Chun-sheng Li

Figure 2. Protein expression of RAS in the pulmonary artery and effects of captopril on APE. A: protein expression and quantitative analysis of RAS in the pulmonary artery and effects of captopril on APE, as revealed by Western blotting analysis; B: immunohistochemistry analysis of protein expression of ACE2 in the pulmonary artery in the control, APE-CA (black arrow pointing to expression of ACE2 in vascular endothelial cells), ROSC-saline (black arrow showing expression of ACE2 in vascular endothelial cells), and ROSC-captopril groups (red arrow showing expression of ACE2 in proliferative endotheliocytes); protein expression of Mas receptor in the pulmonary artery in the control, APE-CA (red arrow showing expression of Mas in proliferative endotheliocytes), ROSC-saline, and ROSC-captopril groups (black arrow showing expression of Mas receptor in vascular endothelial cells; red arrow showing expression of Mas receptor in proliferative endotheliocytes). Compared with the control group, *P<0.05, **P<0.01, ***P<0.001; compared with the APE-CA group, ##P<0.01, P<0.001; compared with the ROSC-saline group, ^P<0.05. Scale bar in B: 100 μm. RAS: renin angiotensin system; APE: acute pulmonary embolism; ACE2: angiotensin-converting enzyme 2; CA: cardiac arrest; ROSC: return of spontaneous circulation.