Concentrations of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) in cerebrospinal fluid of patients with severe head injuries

UZAN M., TANRIÖVER N., TOPAL SARIKAYA A., TANRIVERDİ T., Tuzgen S., Cevherkesin B.

Neurosurgery Quarterly, cilt.13, sa.2, ss.117-124, 2003 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 13 Sayı: 2
  • Basım Tarihi: 2003
  • Doi Numarası: 10.1097/00013414-200306000-00007
  • Dergi Adı: Neurosurgery Quarterly
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.117-124
  • Anahtar Kelimeler: Brain injury, Inducible nitric oxide synthase, Neuronal nitric oxide synthase, Nitric oxide synthase
  • İstanbul Yeni Yüzyıl Üniversitesi Adresli: Evet

Özet

There is growing evidence that nitric oxide (NO) produced by isoforms of nitric oxide synthase (NOS), namely, inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS), plays a role in neuronal damage after neurotrauma. NO is a powerful universal mediator of many biologic reactions, including the mechanisms of injury during head trauma. Understanding of the organization and function of NO and NOS has led to new concepts in the treatment modalities of neuronal damage after head injury. In the current study, nine consecutive patients with a severe head injury who were admitted to Cerrahpasa Medical School Hospital at the University of Istanbul between January 2001 and July 2001 were evaluated. Cerebrospinal fluid (CSF) samples were withdrawn from the intraventricular catheter at admission (4-8 hours after trauma) and on each of the next 3 days. The iNOS and nNOS concentrations were assayed in 72 samples of ventricular CSF. CSF concentrations of iNOS and nNOS were increased after severe closed-head injury and peaked at 64 to 72 hours and 20 to 24 hours after trauma, respectively. These results suggest that maximal neuronal damage may occur between 20 and 24 hours after injury as a result of increased nNOS activity, which may contribute to the concomitant excitotoxic neuronal death after traumatic brain injury.