This review describes the effects of realization of the central and peripheral "
cholinergic antiinflammatory pathway" in a model of endotoxic and
anaphylactic shock. Under endotoxic
shock conditions, a pharmacological correction by means of the central m-
cholinomimetic action (electrical stimulation of the distal ends of nervus vagus after bilateral cervical
vagotomy, surgical implantation of the stimulant devise, activation of efferent vagal neurons by means of
muscarinic agonist) is directed toward the elimination of LPS-
induced hypotension. During the
anaphylaxis, peripheral effects of the
cholinergic system induced by blocking m-AChR on the target cells (neuronal and non-neuronal lung cells) and
acetylcholinesterase inhibition are related to suppression of the bronchoconstrictor response. The role of immune system in the pathogenesis of endotoxic
shock is associated with the production of proinflammatory
cytokines by macrophages, increase in
IgM concentration, and complement activation, while the role in the pathogenesis of
anaphylactic shock is associated with
IgE,
IgG1 augmentation. Effects of B cell stimulation may be important in
hypoxia and in the prophylaxis of stress
ulcers and other diseases.
Plasma proteins can influence the effects of the
muscarinic antagonist methacine:
IgG enhance its action while
albumin and CRP abolish it.