Nivalin stimulates acetylcholine-mediated neurotransmission in the splanchnic nerve to the receptors of adrenal medulla chromaffin cells. The stimulating effect is also exhibited via the blood. The result is release of medullar epinephrine.
Experimental data indicate that subcutaneously administered Nivalin increases significantly plasma 17-oxycorticosteroid concentrations . This effect is realized via the pituitary-adrenal system and stimulation of peripheral cholinergic structures, and ACTH is suggested to play a key role .
Low doses of Nivalin cause accelerated rate of fast potentials and appearance of slow potentials. In higher dose the effect of Nivalin develops in two phases: inhibition, followed by stimulation.
Nivalin potentiates acetylcholine-mediated effects in the heart, expressed in moderate negative inotropism occurring at concentrations of 10-6 to 10-3 g/ml. Higher doses produce a biphasic change in heart rhythm: initially slows down and then becomes faster. This is reflected in moderate PQ-interval elongation and higher T-wave voltage in the electrocardiogram.
Nivalin exhibits moderate hypotensive effects at low and medium doses, potentiating the cardiac and peripheral vascular effects of acetylcholine. At higher doses the effect is byphasic: an initial drop in arterial blood pressure is followed by raised blood pressure, which is explained by the effects of Nivalin on central nervous system, adrenal medulla, sympathetic ganglia and postganglionic parasympathetic conduction in the heart muscle.
Nivalin has no cardiotoxic effect within a broad dosage range. Any adverse effects can be rapidly neutralized by atropine.
Nivalin crosses the blood-brain barrier due to the presence of tertiary nitrogen atom. This enables it to exhibit its anticholinesterase activity at all levels in the central nervous system where acetylcholine-mediated neurotransmission takes place.
Nivalin increases the bio-electrical activity of the spinal cord and medulla. The frequency and amplitude biopotentials in postganglionic fibers increase. Nivalin intensifies efferent activity in the motor nerves.
Nivalin stimulates all monosynaptic and polysynaptic reflexes in the spinal cord. The effects of Nivalin on spinal cord and brain medulla have dual realization - through action and through descending reflex control from central brain structures.
Conditioned reflexes, as a classical model of higher nervous activity, are influenced by Nivalin. Nivalin shortens the latency period and the reaction time for conditional reflexes.
Nivalin abolishes disturbances in the conditional reflex caused by cholinolytics. Animal studies have demonstrated that Nivalin normalizes disturbed function on several levels of higher nervous activity, induced by psychopharmacological agents .
Electroencephalographic (ECG) registration of brain bioelectrical activity has shown that Nivalin acts on the ascending activating reticular formation in brain stem and ventral and dorsal hippocamp. Histologic changes were found in the neuronal cells of these structures, which confirms Nivalin interference in their metabolic activity .
Experimental data show that Nivalin activates phagocytosis and thus improves cell-mediated immunity. This mechanism is thought to be triggered by the effect of Nivalin on central and autonomic nervous system through acetylcholine and other mediators .
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