Tramadol reduces myocardial infarct size and expression and activation of nuclear factor kappa B in acute myocardial infarction in rats

Abstract

Some anaesthetics show cardioprotective properties, but the underlying mechanism remains elusive. The aim of this study was to investigate the cardioprotective effect of tramadol and the association of the effect with the changes in expression and activation of nuclear factor kappa B (NF-kappaB) in acute myocardial infarction in a rodent model. Male Sprague-Dawley rats were randomly divided into three groups: the sham group, exposure of anterior parts of the heart was carried out without ligation of the coronary artery; coronary artery occlusion (CAO) group, ligation of the left anterior descending branch of the coronary artery was performed; and the group in which the animals were pretreated with tramadol (12.5 mg kg(-1), intravenously) before the CAO (T + CAO). The infarct size, expression of NF-kappaB subunit p65 mRNA and protein and intercellular adhesion molecule-1 mRNA were examined. Isolated nucleus suspension was analysed by flow cytometry to determine activation of NF-kappaB. The area at risk (percentage of left ventricle) was 46.4 +/- 6.2 and 48.2 +/- 5.9% in the CAO and T + CAO groups, respectively, showing no statistical difference in area at risk/left ventricle between the two groups (P > 0.05). The infarct size (percentage of risk area) was reduced from 44.9 +/- 6.8% in CAO animals to 31.6 +/- 7.7% in T + CAO animals. The reduction of infarct size in the T + CAO group was statistically significant (P < 0.05). Expression of NF-kappaB and its mRNA and intercellular adhesion molecule-1 mRNA was significantly increased in the CAO group compared with the sham group and was significantly decreased in the T + CAO animals. Flow cytometry assay revealed that tramadol attenuated the activation of NF-kappaB by 13.4%. Tramadol may protect myocardium against acute myocardial ischaemic injury and could reduce myocardial infarct size, which may be associated with the expression and activation of NF-kappaB.