Histochemical changes of NADPH-diaphorase in Guillain–Barre syndrome

The distribution of NADPH-diaphorase activity in peripheral nerve biopsy was studied to evaluate the role of nitric oxide in demyelination. NO is an important inflammatory mediator which appears to exert significant effects in number of demyelinating diseases, and sometimes is established a direct causal link between NO and demyelination. Till now there wasn’t any description for the involvement of nitric oxide in GBS cellular immune reactions. We have studied cellular and subcellular histochemistry of NADPHdiaphorase in GBS. Peripheral nerve biopsy tissues were examined with regard to disease duration, from 6 patients who were 11 to 52 days after onset of symptoms. Tetrazolium method in our modification was used to visualize NADPHdiaphorase reaction in the successive tissue sections on the cellular and ultrastructural levels. We have shown that specific pattern of histochemical reaction was characteristic for each distinct time point of disease duration. Up and downregulation mode of histochemical reaction was different for Schwann cells (SC) and mononuclear inflammatory cells. During demyelination reduced NADPH-diaphorase activity was found in SCs associated with degrading myeline sheath. During remyelination that characterized by proliferation of SCs and enlarge of its cell volume we observed an increase in NADPH-diaphorase reaction that indicated on the rise of the NO production in it. In that activated SCs the intracellular distribution of NADPH-diaphorase is changed. Maximum of reaction intensity was shifted in nucleus. It suggests the appearance of the expressional regulation in SCs, which characteristic for the highoutput iNOS, and directed to increase of NO production The levels of NADPH-diaphorase activity varied in large extend in different recruited macrophages in the same tissue sample. It reflects the cyclic character proper to macrophagal iNOS. Intensive reaction was found in cytoplasm and nuclear envelop of the mononuclear cells, that migrate throw the blood vessel walls where NO may enhancing local nerve blood flow and serve simultaneously as important effector in the clearance of the myelin/axonal debris. High intensive NADPH-diaphorase activity was detected in distinct cytoplasm regions of the macrophage on the territory of the injured myelin sheath. Hyperproduction of nitric oxide and cytotoxic effect may take place in such districts. All this findings suggest that endogenous nitric oxide is involved in pathogenesis of GBS.