J Thorac Cardiovasc Surg 2003;126:1461-1466
© 2003 The American Association for Thoracic Surgery
Cardiopulmonary support and physiology
a Departments of Cardiovascular Surgery, Sendai, Japan
b Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan
c Department of Neurology, Okayama University Graduate School of Medicine, Okayama, Japan
Received for publication October 8, 2002; accepted for publication January 14, 2003.
* Address for reprints: Masahiro Sakkurai, MD, PhD, Department of Cardiovascular Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan
OBJECTIVE: The mechanism of spinal cord injury is believed to be related to the vulnerability of spinal motor neuron cells against ischemia. We tested whether MCI-186, which is useful for treating ischemic damage in the brain, can protect against ischemic spinal cord damage.
METHODS: After induction of ischemia, MCI-186 or vehicle was injected intravenously. Cell damage was analyzed by observing the function of the lower limbs and by counting the number of motor neurons. To investigate the mechanism by which MCI-186 prevents ischemic spinal cord damage, we observed the immunoreactivity of Cu/Zn superoxide dismutase, neuronal nitric oxide synthase, and endothelial nitric oxide synthase.
RESULTS: MCI-186 eased the functional deficits and increased the number of motor neurons after ischemia. The induction of neuronal nitric oxide synthase was significantly reduced by the treatment with MCI-186. Furthermore, the increase in the induction of endothelial nitric oxide synthase and Cu/Zn superoxide dismutase was more pronounced.
CONCLUSION: These results indicate that MCI-186 may protect motor neurons from ischemic injury by reducing neuronal nitric oxide synthase and increasing endothelial nitric oxide synthase. MCI-186 may be a strong candidate for use as a therapeutic agent in the treatment of ischemic spinal cord injury.
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