The aim of the present study was to investigate the effect of nitric oxide inhalation (NOI) on cardiac troponin I (CTnI) levels and mean pulmonary arterial pressure (mPAP) in rabbits with acute massive pulmonary embolism (AMPE). Thirty rabbits were used as animal models for AMPE and received different treatments. A total of 4 h after successful modeling, the control group (CON, n=10) received conventional thrombolysis, whereas the treatment group (TRE, n=10) received conventional thrombolysis plus NOI. The experimental group (EXP, n=10) did not receive any treatments. Myocardial necrosis was pathologically confirmed in all 30 rabbits. In group EXP, the post-AMPE CTnI peak level was 0.42 +/- 0.12 mu g/l, was achieved in 18.8 +/- 4.5 h and remained positive for 38.6 +/- 5.2 h (>= 0.1 mu g/l). These values were lower in group TRE when compared with those in groups CON and EXP (P<0.05). Group TRE exhibited significantly reduced mPAP at 24, 28, 32, and 34 h (P<0.05) when compared with group CON. AMPE-induced cardiac impairment was more severe in group EXP when compared with groups CON and TRE. The present findings indicated that the CTnI peak was significantly correlated with the corresponding mPAP. Furthermore, the results suggested NOI may reduce mPAP and CTnI peak levels, with protective effects against AMPE-induced myocardial damage in rabbits.