Background This study aimed to investigate the effects of brain natriuretic peptide(BNP) on myocardial ischemiareperfusion(I/R) injury in rats in vivo.Method Twenty-one,male,Sprague-Dawley rats were randomly divided into three groups:(1) the sham operated group(SHAM) underwent thoracotomy without ligation of the coronary artery;(2) in the I /R group,the left anterior descending coronary artery was ligated for 35 min and then released to get reperfusion for 4 h;(3) in the BNP group,BNP was continuously infused 10 min after the ligation at a rate of 0.01 μg /kg /min.Then the left anterior descending coronary artery was ligated for 35 min and released to get reperfusion for 4 h.The infusion of BNP was maintained until the end of reperfusion.The myocardial infarction area in each group was determined using the 1,2,3,5-triphenyltetrazolium staining method to measure the extent of myocardial I/R injury in rats.Myocardial apoptosis was detected using the terminal deoxynucleotidyl transferase mediated dUTP-biotin nick endlabeling(TUNEL) method.Results No myocardial infarction was observed in the SHAM group.The myocardial infarction size was 44.79 ± 7.44% in the I/R injury group and 19.72 ± 5.49% in the BNP group(P < 0.01).The apoptosis indices of the SHAM,BNP,and I /R groups were 5.37 ± 4.21%,22.50 ± 9.50 %,and 45.24 ± 13.01 %,respectively(P < 0.01).Conclusions BNP can decrease the myocardial infarction size caused by I/R injury in rats in vivo.This finding may be accounted for by the fact that BNP decreases myocardial apoptosis induced by I/R injury. Background This study aimed to investigate the effects of brain natriuretic peptide (BNP) on myocardial ischemiareperfusion (I / R) injury in rats in vivo. Method Twenty-one, male, Sprague-Dawley rats were differentiated into three groups: (1) the sham operated group (SHAM) underwent thoracotomy without ligation of the coronary artery; (2) in the I / R group, the left anterior descending coronary artery was ligated for 35 min and then released to reperfusion for 4 h; (3) in the BNP group, BNP was continuously infused for 10 min after the ligation at a rate of 0.01 μg / kg / min. The left anterior descending coronary artery was ligated for 35 min and released to get reperfusion for 4 h. The infusion of BNP was maintained until the end of reperfusion. The myocardial infarction area in each group was determined using the 1,2,3,5-triphenyltetrazolium staining method to measure the extent of myocardial I / R injury in rats. Myocardial apoptosis was detected using the terminal deoxynucleotidyl transferase mediated dUTP-biotin nick endlabeling (TUNEL) method. Results No myocardial infarction was observed in the SHAM group. The myocardial infarction size was 44.79 ± 7.44% in the I / R injury group and 19.72 ± 5.49% in the BNP group (P < 0.01). The apoptosis indices of the SHAM, BNP, and I / R groups were 5.37 ± 4.21%, 22.50 ± 9.50%, and 45.24 ± 13.01%, respectively (P <0.01) .Conclusions BNP can decrease the myocardial infarction size caused by I / R injury in rats in vivo. This finding may be accounted for the fact that BNP decreased myocardial apoptosis induced by I / R injury.