Imbalance of angiotensin-converting enzymes affects myocardial apoptosis during cardiac arrest induced by acute pulmonary embolism in a porcine model

Figures

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  Figure 1. Histological analysis following APE-CA and ROSC and the effects of captopril. Representative images of H&E-stained myocardial tissues (magnification, ×100). Black arrows indicate fractured myocardial fibers. APE-CA, acute pulmonary embolism with cardiac arrest; ROSC, return of the spontaneous circulation; Cap, captopril; SA, saline.

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  Figure 2. Cytoplasmic ultrastructure of the myocardium viewed under a transmission electron microscope at high magnification (×20,000). Black arrows indicate myocardial fibers and the junction between myocardial cells called intercalated discs that are broken or dissolved. Red arrows indicate apoptotic cells. Treatment with captopril decreased the number of apoptotic cells in the left myocardium. APE-CA, acute pulmonary embolism with cardiac arrest; ROSC, return of the spontaneous circulation; Cap, captopril; SA, saline.

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  Figure 3. Expression of proteins of the RAS in the left myocardium as determined by (A and B) WB analysis and (C) immunohistochemistry (scale bar, 100 µm; black arrows indicate expression of the Mas receptor). (D and E) Expression of members of the RAS in the right myocardium as determined by WB analysis. Vertical lines in the western blot indicate non-adjacent bands from the same gel. Values are expressed as the mean ± standard deviation, N=5 pigs per group. *P<0.05; **P<0.01; ***P<0.001 vs. control group; #P<0.05; ##P<0.01; ###P<0.001 vs. the APE-CA group; &&&P<0.001 vs. the ROSC-SA group; APE-CA, acute pulmonary embolism with cardiac arrest; ROSC, return of the spontaneous circulation; SA, saline; ACE, angiotensin-converting enzyme; RAS, renin-angiotensin system; IHC, immunohistochemistry; AT1, angiotensin II receptor type 1; WB, western blot.

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  Figure 4. Differences in expression of proteins of the renin-angiotensin system between the left and right myocardium in APE-CA. (A) ACE, (B) AT1 receptor, (C) Mas receptor and (D) ACE2/ACE ratio. N=5 pigs per group. *P<0.05; **P<0.01; ***P<0.001 vs. the control group; #P<0.05; ###P<0.001 vs. the APE-CA group. APE-CA, acute pulmonary embolism with cardiac arrest; ROSC, return of the spontaneous circulation; SA, saline; ACE, angiotensin-converting enzyme; AT1, angiotensin II receptor type 1.

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  Figure 5. Expression of apoptotic signaling proteins in the left and right heart as determined by WB. (A) Representative images and quantitative analysis of Bax, Bcl-2 and caspase-3 in the left heart. (B) Representative images and quantitative analysis of Bax and cleaved caspase-3 in the right heart. Vertical lines in the western blot indicate non-adjacent bands from the same gel. N=5 pigs per group. *P<0.05; **P<0.01; ***P<0.001 vs. the control group; #P<0.05; ##P<0.01; ###P<0.001 vs. the APE-CA group; &P<0.05; &&P<0.01; &&&P<0.001 vs. the ROSC-SA group. APE-CA, acute pulmonary embolism with cardiac arrest; ROSC, return of the spontaneous circulation; SA, saline; WB, western blot; Cap, captopril; Bcl-2, B-cell lymphoma 2; Bax, Bcl-2-associated X.

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  Figure 6. ACE2/ACE axis imbalance and apoptotic signaling proteins, and p-ERK1/2 in the left myocardium of APE-CA and ROSC pigs as determined by immunohistochemistry. (A) Correlation between the ACE2/ACE axis and apoptosis-associated proteins. (B) Representative images. Black arrows indicate staining for p-ERK1/2 (scale bar, 100 µm). (C) Quantitative analysis of immunohistochemical staining. N=5 pigs per group. **P<0.01; ***P<0.001 vs. the control group; #P<0.05; ##P<0.01 vs. the APE-CA group; &P<0.05 vs. the ROSC-SA group. APE-CA, acute pulmonary embolism with cardiac arrest; ROSC, return of the spontaneous circulation; SA, saline; Cap, captopril; p-ERK, phosphorylated extracellular signal-regulated kinase.