Apoptotic change and NOS activity in the experimental animal diffuse axonal injury model

Although nitric oxide (NO) plays an important role in the pathophysiologica l process of cerebral ischemia or severe traumatic brain injury, its contri bution to the pathogenesis of moderate diffuse axonal injury (mDAI) remains to be clarified. The alterations in nitric oxide synthase (NOS) activity a nd the histopathological response after mDAI was investigated. Forty anesth etized Sprague-Dawley adult rats were injured with a Marmarou's weight-drop device through a Plexiglas guide tube. These rats were divided into 8 grou ps (control, 1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 48 hr after trauma). The temporal pattern of apoptosis in the adult rat brain after mDAI was charac terized using TUNEL histochemistry. In addition, the cDNA for NOS activity was amplified using RT-PCR. The PCR products were electrophoresed on a 2% a garose gel. eNOS activity was not detected, but nNOS activity was expressed after 3 hr and continuously 48 hr after impact, which was approximately do uble that of the control group at 12 and 24 hr. Subsequently, there was a d ecrease in activity after 48 hr. The iNOS activity increased dramatically a fter 12 hr and was constant for a further 12 hr followed by a dramatic decr ease below the level of the control group. Significant apoptotic changes oc curred 12 and 24 hr. after insult. nNOS and iNOS activity were affected aft er moderate diffuse axonal injury in a time-dependent manner and there was a close relation between the apoptotic changes and NOS activity. Although t he nNOS activity was expressed early, its activity was not stronger than iN OS, which was expressed later.