Nitric oxide (NO) is a gaseous mediator which modulates functions of immune system, the vascular tone and neuronal functions. The aim of this study was to evaluate the role of NO as a relevant mediator in the pathogenesis of Guillan-Barré syndrome (GBS). We measured the serum concentration of NO 2/NO 3 and the level of inducible NO synthase (iNOS) in circulating monocytes of 10 patients affected by GBS, before the start of pharmacological treatment. The NO 2/NO 3 plasmatic concentration were assayed by optical enzyme assay by using nitrate reductase. The analysis of iNOS transcript in circulating monocytes performed by reverse transcriptase polymerase chain reaction (RT-CPR). The NO 2/NO 3 concentration in the plasma of GBS patients was, respectively, 10k and 12-fold higher than the amount in a pool of 22 patients with diseases of the peripheral nervous system and 20 normal healthy subjects. The analysis of iNOS mRNA in circulating monocytes showed a specific transcript in GB patients, whereas this was absent in the monocytes of the two control groups. The data suggest that NO may be a mediator of myelin damage in GBS. We can speculate that the vasodilating effect of NO could participate to the blood nerve barrier modification which is instrumental in the recruitment of lymphomononuclear cells; alternatively NO could act as a free radical, thus causing a direct myelin injury.
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
ASJC Scopus subject areas
- Clinical Neurology