The adenosine triphosphate-sensitive potassium channel opener nicorandil protects the ischemic rabbit spinal cord

We investigated the protective effects of an adenosine triphosphate-sensitive potassium channel opener nicorandil in the rabbit model of spinal cord ischemia.

Rabbits were randomized into 4 groups (each n = 6): the nicorandil group (100 microg/kg intravenous nicorandil 10 minutes before ischemia); the glibenclamide plus nicorandil group (3 mg/kg intravenous glibenclamide, an antagonist of adenosine triphosphate-sensitive potassium channels, 10 minutes before nicorandil administration); the vehicle group (vehicle alone); and the sham operation group (without spinal cord ischemia). Spinal cord ischemia was induced by balloon occlusion of the infrarenal abdominal aorta for 15 minutes at 39 degrees C. Neurologic function was graded into Johnson's score at 8 hours, 1 day, and 2 days. Histopathologic examination was performed at 2 days, and the number of intact motor neuron cells was compared.

Johnson scores of the glibenclamide plus nicorandil and vehicle groups were significantly lower than those of the sham operation and nicorandil groups at each time point, and no statistically significant difference was observed between the glibenclamide plus nicorandil and vehicle groups. Histopathologic examination revealed that motor neurons were almost normal in the nicorandil group, whereas about 55% of motor neurons were lost in the vehicle and glibenclamide plus nicorandil groups.

Nicorandil has a protective effect on the ischemic rabbit spinal cord, and the beneficial effect seems mediated through the activation of adenosine triphosphate-sensitive potassium channels.