Acute pulmonary embolism (APE) is frequently reported in patients with cardiac arrest (CA) in emergency care. Pneumocyte apoptosis is commonly observed in the lungs following an APE. An important pathological mechanism evoking apoptosis during a lipopolysaccharide-induced acute lung injury is the angiotensin-converting enzyme 2 (ACE2)/ACE imbalance. The present study uses a porcine model to examine the anti-apoptotic effects of captopril on APE-CA and the return of spontaneous circulation (ROSC). Pigs were randomly assigned into four groups: Control, APE-CA, ROSC-saline, and ROSC-captopril. Surviving pigs were euthanized at 6 h and lungs were isolated for analysis using several biochemical assays. Compared with the control group, the ACE2/ACE ratio was lower in the APE-CA and ROSC pigs. In addition, APE-CA pigs had higher Bcl-2-associated X protein (Bax) and cleaved caspase-3 levels, and lower B-cell lymphoma-2 (Bcl-2) level compared to control pigs. Captopril treatment reduced lung apoptosis, as demonstrated by lower TUNEL-positive cells, higher Bcl-2, and lower cleaved caspase-3 protein levels in the lung. Notably, the ACE2/ACE ratio was positively correlated with Bcl-2 protein levels and Bcl-2/Bax ratio. In conclusion, captopril has a protective effect against lung apoptosis following ROSC and that maintaining the balance of the ACE2/ACE axis is important for inhibiting pulmonary apoptosis during APE.