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At least 217 records · Page 12Linked to original sources
PubMed1997

Sodium channels and therapy of central nervous system diseases.

Voltage-dependent Na+ channels have long been recognized targets for anti-arrhythmic and local anesthetic drugs. Since the mid-1980s, Na+ channels have become widely accepted as the primary target of anticonvulsants with pharmacological profiles similar to phenytoin, carbamazepine, and lamotrigine. Results from animal models and a few preliminary clinical trials suggest that this class of drugs may also offer significant potential for reducing the neuronal damage caused by ischemic stroke, head trauma, and perhaps certain neurodegenerative diseases. Studies using site-directed mutations of Na+ channels with electrophysiology have provided extensive insight into both the physiology and the interaction of drug molecules with ion channels. This review includes an introduction to Na+ channel structure, molecular biology, and physiology as they relate to pharmacology. A review of several in vitro actions of Na+ channel blockers is provided. Neuroprotective actions with a variety of Na+ channel blockers in models of central nervous system disease in animals and in vitro models are reviewed. Although many voltage-dependent Na+ channel blockers have additional pharmacological targets, the hypothesis that anticonvulsant and neuroprotective actions results from the blockade of Na+ channels is explored.

Amino Acid Sequence↗
PubMed1997

[Patterns in the change of the evoked skin autonomic potential in nervous system diseases].

The study of sympathetic skin response (SSR) was performed both in 30 healthy volunteers either in rest or after pharmacological preparations administration (reserpine, sydnocarb, gammalone) and in 48 patients with autonomic disfunction, syringomyelia, polyneuropathy. It was determined that two processes were presented in SSR structure, exactly: the first one which included I and III phases and was bound with trophotropic functions and the second process which was presented by II phase only and reflected the activity of ergotropic functions. The latent period of SSR reflected the tonus of the sympathetic nervous system. It was established that SSR changed regularly in the nervous systems diseases studied: thus, increase or decrease of the latent period as well as of the amplitudes of SSR phases were observed in autonomic disfunction while depression or absence of SSR took place in syringomyelia or polyneuropathies. The data obtained testified the results of the other authors about possibility of SSR usage for diagnosis of both central and peripheric autonomic disturbances.

Adolescent↗
PubMed2004

Isoprostanes as biomarkers and mediators of oxidative injury in infant and adult central nervous system diseases.

Isoprostanes are a family of prostaglandin-like compounds that are generated in vivo by free radical attack of esterified arachidonic acid and then released in free form in biological fluids. Since their discovery in 1990, they have been extensively used as biomarkers of lipid peroxidation and oxidative damage in an increasing number of human diseases. Few members of the isoprostane family are biologically active and could contribute to the functional consequences of oxidant injury. The present review summarises the current knowledge on formation and biological activities of these lipid peroxidation products, focusing on their role as valuable biomarkers to investigate the involvement of oxidative stress in the pathogenesis of infant and adult central nervous system diseases. In addition to isoprostanes, a new class of free radical-mediated peroxidation products, named neuroprostanes, is discussed. Neuroprostanes derive from peroxidation of docosahexaenoic acid, a polyunsatured fatty acid particularly abundant in neurons, and may represent a more selective index of brain oxidant injury than isoprostanes. In spite of some discrepancies in the results reported in different studies, isoprostane and neuroprostane levels in human biological fluids, as well as in experimental models of brain diseases, appear to be valuable indicators not only to monitor the occurrence and the causal role of oxidative stress in brain pathologies, but also for critical selection and evaluation of appropriate antioxidant therapies.

Adult↗