For improved neurotransmission!
Nivalin is the result of a natural product developed on the basis of an extract from Galanthus Nivalis!
Nivalin is applicable in medical practice wherever there is a need for stimulation and potentiation of synaptic acetylcholine-mediated neurotransmission. Initially, Nivalin was used in anesthesiology to antagonize the effects of non-depolarizing muscle relaxants , and since then it was rapidly introduced in other areas of medicine, i.e. neurology, ophthalmology, gastroenterology, intensive care and resuscitation, cardiology, physiotherapy.
Nivalin is a product with broad therapeutic index, allowing "soft" manifestation of its effect with individual dosing depending on the particular case.
Galantamine hydrobromide (Nivalin) has empirical formula [C17H21NO3].HBr and molecular weight 386.3. The dry substance is a microcrystalline powder, odorless. It is very soluble in water and practically insoluble in organic solvents. Nivalin is an alkaloid, which chemically is a derivative of phenanthredine with tertiary ammonium radical, allowing its passage through the blood-brain barrier. Aqueous solutions of Nivalin have pH 6.2.
Nivalin binds electrostatically to the enzyme active site of cholinesterase. Binding is reversible, thus it acts as a competitive reversible inhibitor of cholinesterase and prolongs the hydrolysis of endogenous acetylcholine, thereby increasing its accumulation and prolonging and potentiating its effects, which are expressed in intensified and prolonged mediation at the level of cholinergic postsynaptic membrane, Fig. 2. Nivalin has been found to exert direct effect on some CNS structures with cholinergic neurons. It also acts in CNS by reflex pathway, potentiating afferent impulses from some peripheral reflexogenic areas, Fig. 3.
Nivalin inhibits reversibly brain, erythrocytic, muscle and serum cholinesterase. Its effect on brain cholinesterase is 10-12 times as potent, compared to physostigmine, since Nivalin crosses the blood-brain barrier. Galanthamine hydrobromide (Nivalin) inhibits muscle cholinesterase more potently than pyridostigmine bromide and more weakly than neostigmine bromide. The anticholinesterase activity of Nivalin occurs at concentrations above 10 -17 g/ml.
Nivalin prolongs the action of acetylcholine on postsynaptic membranes and its accumulation in the synaptic gap, thereby increasing the intensity and duration of nerve impulse transmission to muscle tissues. The strength and duration of muscle contraction increases. This effect is dependent on Nivalin concentration, respectively on its plasma level.
Nivalin found its first clinical application in anaesthesiology as an agent to antagonise the effects of non-depolarizing neuromuscular blockers, such as d-tubocurarine, gallamine, pancuronium bromide, Alloferin, Diplacin.
By blocking acetylcholinesterase, Nivalin enables acetylcholine to replace a neuromuscular blocker from postsynaptic membrane receptors and thus restore neuromuscular transmission.
The antagonistic effect develops 20 - 30 s after Nivalin administration. It is stable in time, as the steady-state lasts 30 - 60 min. No phenomena of recurarizing are observed.
Nivalin has milder and more easily controllable effect that neostigmine: broader therapeutic index, mild cardiotoxicity, and less potently expressed muscarinic and parasympathomimetic effects. <
Nivalin is convenient and suitable for administration to children and elderly patients.
Nivalin potentiates neuromuscular blockade induced by depolarizing blocking agents (succinylcholine).
Once depolarized by the respective depolarizing muscle relaxant, the postsynaptic membrane continues to depolarize, i.e. depolarization is maintained by acetylcholine cumulation induced by Nivalin.
Nivalin should not be administered with or whenever depolarizing neuromuscular blockers have been used! 
Nivalin stimulates gastrointestinal musculature. It increases the tone and frequency of smooth muscle contractions. It activates motility and peristalsis. This phenomenon induced by Nivalin is often a desired necessity, as it can be controlled by flexible dosage and neutralized with parasympatholytics (atropine) .
Nivalin increases the tone of the bladder detursor muscle and decreases its excitability threshold 15-20 times. Nivalin potentiates the myoelectric stimulation of bladder detrusor function. Nivalin increases the tone and peristalsis of ureters, whereby relieving and facilitating urinary outflow.
Nivalin prolongs, intensifies and increases the amplitude of postganglionic potentials. It mildly decreases negative after-potentials. Nivalin antagonizes the ganglion-blocking effect of hexamethonium on synaptic transmission in the upper cervical sympathetic ganglia.
Nivalin increases the sensitivity of acetylcholine chemoreceptors in the carotid sinus. It stimulates afferent impulses in Hering's nerve and thus stimulates respiration.
Nivalin antagonizes the blocking effect of curare and curare-like nondepolarizing drugs on the carotid sinus.
Nivalin exerts direct effect on acetylcholine-mediated chemoreceptors on the carotid sinus. Experimental data have shown that it potentiates the stimulating effect of nicotine and potassium cyanide on the carotid sinus .
These effects of Nivalin are exhibited in concentrations of 5 x 10-7 - 10-4g/ml.
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