Résumé
BACKGROUND: Production of nitric oxide (NO) radicals may contribute to neuronal injury. We examined that the inhibition of NO synthase (NOS) could improve postischemic neurologic outcome after spinal cord ischemia in rabbits. Also, we measured cGMP as a marker of NOS activation in control and experimental groups. METHODS: Spinal cord ischemia in rabbits was induced by aortic occlusion with aneurysm clip at the level just below branching of left renal artery. Five minutes before aortic occlusion, saline (control group, n=10) or a NOS inhibitor NG-nitro-L-arginine methyl ester (10 mg/kg, L-NAME group, n=10) was injected intravenously. After 15 min ischemia and 1 hour reperfusion, animals were sacrified and the spinal cords were extruded for the measurement of cGMP by enzymeimmunoassay. For neurologic examination, the same procedures of ischemia/reperfusion and drug injection were done, except that rabbits were perfused for 4 hours (control-4 and L-NAME-4, n=8 at each group) or 48 hours (control-48 and L-NAME-48, n=8 at each group) after aortic occlusion. RESULTS: L-NAME (10 mg/kg) increased mean systemic arterial pressure accompanied by bradycardia, and reduced cGMP significantly. Control-4 animals showed better neurologic function than L-NAME-4 animals (p<0.05), however, there was no significant difference of neurologic outcome between control-48 and L-NAME-48 groups. CONCLUSION: Intravenous administration of L-NAME prior to spinal cord ischemia/reperfusion diminishes the extent of postischemic neuronal spinal cord damage at the early postreperfusion period.
Sujets)
Animaux , Lapins , Administration par voie intraveineuse , Anévrysme , Pression artérielle , Bradycardie , Ischémie , Examen neurologique , Neurones , L-NAME , Monoxyde d'azote , Nitric oxide synthase , Nitroarginine , Artère rénale , Reperfusion , Ischémie de la moelle épinière , Moelle spinaleRésumé
BACKGROUND: Production of nitric oxide (NO) radicals may contribute to neuronal injury. We examined that the inhibition of NO synthase (NOS) could improve postischemic neurologic outcome after spinal cord ischemia in rabbits. Also, we measured cGMP as a marker of NOS activation in control and experimental groups. METHODS: Spinal cord ischemia in rabbits was induced by aortic occlusion with aneurysm clip at the level just below branching of left renal artery. Five minutes before aortic occlusion, saline (control group, n=10) or a NOS inhibitor NG-nitro-L-arginine methyl ester (10 mg/kg, L-NAME group, n=10) was injected intravenously. After 15 min ischemia and 1 hour reperfusion, animals were sacrified and the spinal cords were extruded for the measurement of cGMP by enzymeimmunoassay. For neurologic examination, the same procedures of ischemia/reperfusion and drug injection were done, except that rabbits were perfused for 4 hours (control-4 and L-NAME-4, n=8 at each group) or 48 hours (control-48 and L-NAME-48, n=8 at each group) after aortic occlusion. RESULTS: L-NAME (10 mg/kg) increased mean systemic arterial pressure accompanied by bradycardia, and reduced cGMP significantly. Control-4 animals showed better neurologic function than L-NAME-4 animals (p<0.05), however, there was no significant difference of neurologic outcome between control-48 and L-NAME-48 groups. CONCLUSION: Intravenous administration of L-NAME prior to spinal cord ischemia/reperfusion diminishes the extent of postischemic neuronal spinal cord damage at the early postreperfusion period.