OBJECTIVE

To investigate the cardioprotective effects of sodium ferulate (SF) mediated by nitric oxide on ischemia-reperfusion injured myocardium.

METHODS

Fifty-six SD rats were killed. Their hearts were isolated and randomly divided into 7 equal groups: ischemia/reperfusion group (I/R group), ischemic/preconditioning (IP group, to be perfumed with anoxic and reoxygenated fluid several times so as to produce protection against continuous and severe ischemia), SF pretreatment group (to be perfused with fluid with SF and then made I/R model), L-NAME + SF group (to be perfused with fluid with SF and L-NAME, a NO inhibitor, and then made I/R model), glibenclamide (Glib) + SF group (to be perfused with Glib + SF and then made I/R model)), L-NAME + Glib + SF group (to be perfused with L-NAME + Glib + SF and then made I/R model)), and control group (normal isolated hearts). Electrocardiography was conducted and left ventricular systolic pressure (LVSP), dp/dt(max), and heart rate (HR) were measured. By the end of the experiment 0.5 grams of tissue was taken from the left ventricle. The levels of superoxide dismutase (SOD), malonyldialdehyde (MOD), NO, and cyclic guanosine monophosphate (cGMP) were detected.

RESULTS

The levels of LVSP, dp/dt(max), and HR of the SF pretreatment group and IP group were all significantly higher than those of the I/R group (all P < 0.01) without significant differences between these 2 groups (all P > 0.05). The levels of LVSP, dp/dt(max), and HR of the L-NAME, Glib + SF, and L-NAME + Glib + SF groups were all significantly lower than those of the SF pretreatment group and IP group (all P < 0.01). Ventricular extrasystole (VE) and ventricular tachycardia (VT) during re-perfusion period occurred in all hearts of the I/R group, however, the incidence rates of VE and VT of the IP and SF groups were all significantly lower than those of the I/R group (all P < 0.01), however, without significant differences between the IP and SF groups (all P > 0.05). The incidence rate of VE and VT of the L-NAME, Glib + SF, and L-NAME + Glib + SF groups were all significantly higher than those of the SF group (all P < 0.01). The myocardium MDA content of the I/R group was significantly higher and the SOD activity significantly lower in comparison with the control group (both P < 0.01); the myocardium MDA contents of the IP and SF groups were significantly lower and the SOD activity levels significantly higher in comparison with the I/R group (all P < 0.01), however, with significant differences between theses 2 groups (both P > 0.05); the myocardium MDA contents were significantly higher and the SOD activity levels significantly lower in the L-NAME, Glib + SF, and L-NAME + Glib + SF groups in comparison with the SF and IP groups (all P < 0.01). The myocardium NO(2)(-)/NO(3)(-) and cGMP contents of the I/R group were both significantly lower than those of the control group (both P < 0.01), and the myocardium NO(2)(-)/NO(3)(-) and cGMP contents of the IP and SF groups were both significantly higher than those of the I/R group (both P < 0.01), however, without significant differences between these 2 groups (both P > 0.05). The myocardium NO(2)(-)/NO(3)(-) and cGMP contents of the L-NAME, Glib + SF, and L-NAME + Glib + SF groups were all significantly lower than those of the SF group (all P < 0.01).

CONCLUSION

SF pretreatment significantly improves the releasing of NO, decreases oxygen free radicals, and relieves myocardial ischemia reperfusion injury. The opening of the ATP-sensitive potassium channels induced by the cGMP way of NO activation may be an important pathway in the cardioprotective effects of SF pretreatment.