Nitric oxide in cerebrospinal fluid and local inducible nitric oxide synthase after cauda equina compression in rats

Abstract

We investigated the time course of changes in nitric oxide metabolite (NO2- plus NO3-: NOx) levels in the cerebrospinal fluid and the expression of local inducible nitric oxide synthase following cauda equina compression in rats. Cerebrospinal fluid NOx levels were significantly increased from 12 h to 3 days after compression, and decreased thereafter. Histologically, inducible nitric oxide synthase immunoreactivity was observed in macrophages that infiltrated the dura mater on days 1 and 3 after compression, but not in foamy macrophages in the parenchyma of the cauda equina observed afterwards. The pattern of NOx levels coincided with the appearance of inducible nitric oxide synthase labeled macrophages, indicating a critical role of these cells as the main synthesizers of NOx in the acute stage of cauda equina compression.

Clinical significance of cerebrospinal fluid nitric oxide concentrations in degenerative cervical and lumbar diseases

“…These findings suggest that the [NOx] increases with chronic, but not subacute, spinal cord or cauda equina compression. In an animal experiment, we previously demonstrated that iNOS is expressed in macrophages and Schwann cells at the cauda equina compression site in rats [10]. Levy et al observed iNOS expression following chronic constriction injury to the sciatic nerve in rats [20].…”

“…Furthermore, the [NOx] in patients with SCI correlates with neurologic severity and recovery rate postoperatively, or with conservative treatment [9]. In animal models, inducible NO synthase (iNOS) is expressed in macrophages and Schwann cells at the cauda equina compression site [10] and in macrophages in the early stages after SCI [7]. Excessive NO production derived from iNOS has cytotoxic effects [11] and induces neuronal apoptosis secondary to neural degeneration and neurodysfunction [12].…”