Nitric Oxide (NO) has been implicated as a mediator of neuronal injury in vascular
stroke. On the other hand, NO is suggested to play a neuroprotective role by increasing blood flow during
cerebral ischemia. In order to evaluate the role of NO in the
spinal cord ischemia, effects of
nitric oxide synthase (NOS) inhibition on the recovery of reflex potentials after a transient
spinal cord ischemia were examined in
urethane-
chloralose anesthetized spinal cats.
Spinal cord ischemia was produced by occlusion of the thoracic aorta and the both internal mammary arteries for 10 min. Regional blood flow (RBF) in the spinal cord was continuously measured with a
laser-Doppler flow meter. The monosynaptic (MSR) and polysynaptic reflex (PSR) potentials elicited by electrical stimulation of the tibial nerve, were recorded from the L7 or S1 ventral root. The recovery process of spinal reflex potentials was reproducible when the oclusion was repeated twice at an interval of 120 min. Pretreatment with N(G)-monomethyl-
L-arginine (
L-NMMA, 10 mg/kg), a NOS inhibitor significantly accelerated the recovery of PSR potentials after
spinal cord ischemia. The accelerating effect of
L-NMMA on the recovery of PSR potentials was abolished by co-administration of
L-arginine (1 mg/kg/min) but not by that of D-
arginine (1 mg/kg/min).
L-NMMA failed to improve RBF in the spinal cord during
ischemia and reperfusion.
Nitroprusside (10 microg/kg/min), a NO donor, retarded the recovery of PSR potentials after
spinal cord ischemia. These results suggest that NO production has a significant influence on the functional recovery after transient
spinal cord ischemia.