The role of constitutive XXXX synthase in pathogenesis of secondary lesion after @entity1566 . Preliminary results.

@entity32 @entity35 @entity1506 @entity2824 @entity842 @entity1566 @entity204 @entity130
BACKGROUND: Secondary lesion (SL) is an early @entity204 following @entity1566 ( @entity1566 ). @entity842 (NO) could be involved in its pathogenesis. NO is a gaseous metabolite produced by 2 constitutive isoforms of NO synthase ( @entity2824 ), constantly active, and by 1 inducible isoform (iNOS), synthesized during @entity32 and able to produce large amount of NO. High concentrated NO is toxic for cells; therefore, NO concentration is strictly and finely regulated. We suppose that major inhibitory effect on the iNOS expression is represented by the same physiological concentration of NO, synthesized by @entity2824 . The aim of this study is to assess the role of the 2 @entity2824 in pathogenesis of SL after @entity1566 in @entity35 . METHODS: A dorsal @entity1566 has been performed on @entity35 (n=5) by a vascular clip (50 g/mm(2) for 15"). Fifteen minutes after @entity130 , activity of nNOS and eNOS has been measured (U/mg) in the cervical, dorsal and lumbar segments of spinal cord. Uninjured @entity35 (n=5) served as control group. m-RNA for iNOS in untreated @entity35 (n=2) has been also investigated by Northern blotting. RESULTS: In injured @entity35 nNOS activity has shown a reduction in dorsal and lumbar segments, compared to the control group. eNOS activity, highly variable in the control group, has not been detectable in injured spinal cord. @entity1506 mRNA has not been found in spinal cord of uninjured @entity35 . CONCLUSIONS: These results would be in line with our hypothesis and provide the bases for other investigations. New therapeutic strategies for SL prevention, based on the modulation of @entity2824 , will be evaluated.
