Nitric oxide and carbon monoxide in the brain pathology of heat stress.

Publisher Summary This chapter focuses on the involvement of nitric oxide (NO) and carbon monoxide (CO) in the brain pathology of heat stress, which is based on immunohistochemical investigations of nitric oxide synthase (NOS) and heme oxygenase (HO) expression in a rat model. To understand the contribution of NO and CO in brain pathology, the influence of selective neuroprotective drugs on NOS and HO expression is examined in this model. These two gaseous molecules are considered as putative neurotransmitters, because they influence intracellular signal transduction mechanisms by freely diffusing from one cell to another. However, unlike the conventional neurotransmitters, these molecules are not stored in synaptic vesicles and their release is not influenced by exocytosis following membrane depolarization. Overproduction of NO seems to be instrumental in various brain diseases. Induction of human inducible NOS occurs in multiple sclerosis, which is mainly found in the areas exhibiting demyelination. In cell culture studies, NO is involved in the pathogenesis of Alzheimer's disease and AIDS dementia. Results demonstrate that hyperthermia associated with heat exposure has the capacity of inducing upregulation of neuronal NOS and HO-2 immunoreactivity in the central nervous system. This induction of NOS and HO in neurons can be prevented by prior treatment with several neuroprotective drugs influencing microvascular permeability, edema, and cell reaction.