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Peripheral neuromuscular

Kao CY, Nishiyama A (1965) Actions of saxitoxin on peripheral neuromuscular systems. J Physiol 180 50-66... [Pg.117]

All these exclude the possibility of a direct effect of 1-phenylsilatrane on the peripheral neuromuscular apparatus. [Pg.81]

The insect GABA receptor-chloride ionophore complex is found in the CNS and also at peripheral neuromuscular sites. GABA receptors belong to a superfamily of ligand-gated ion channels known as Cys-loop receptors that include nicotinic acetylcholine receptors and glutamate-gated chloride channels (Lester, 2004). Cys-loop receptors are so named because... [Pg.127]

Exposure should be terminated as soon as possible either by removal of the patient or by fitting the patient with a gas mask if the atmosphere remains contaminated. Contaminated clothing should be removed immediately the skin and mouth should be washed with copious amounts of water. Gastric lavage should be conducted if necessary. Artificial respiration should be administered if required, and administration of oxygen may be necessary. If the convulsion persists, diazepam (5-10 mg intravenously) or sodium thiopental (2.5% intravenously) should be administered, and the patient should be treated for shock. Atropine should be administered in sufficiently large doses, but atropine is without any effect against peripheral neuromuscular activation and subsequent paralysis. Pralidoxime (1 or 2 g infused intravenously) should be administered for all the peripheral effects. [Pg.34]

The binding of nerve agent to the enzymes is considered irreversible unless removed by therapy. The accumulation of acetylcholine in the peripheral and central nervous systems leads to depression of the respiratory center in the brain, followed by peripheral neuromuscular blockade causing respiratory depression and death. [Pg.1251]

The binding of the nerve agent to the enzyme is considered irreversible unless removed by therapy. The accumulation of acetylcholine in the peripheral nervous system and central nervous system (CNS) leads to depression of the respiratory center in the brain, followed by peripheral neuromuscular blockade causing respiratory depression and death. The pharmacologic and toxicologic effects of the nerve agents are dependent on their stability, rates of absorption by the various routes of exposure, distribution, ability to cross the blood-brain barrier, rate of reaction and selectivity with the enzyme at specific foci, and their behavior at the active site on the enzyme. [Pg.2848]

Maksymowych, A.B., Reinhard, M., Malizio, C.J., Goodnough, M.C., Johnson, E.A., and Simpson, L.L. 1999. Pure botulinum neurotoxin is absorbed from the stomach and small intestine and produces peripheral neuromuscular blockade. Infect. Immun. 67 4708 4712. [Pg.418]

Hypocalcemia may manifest as neuromuscular, CNS, dermatologic, and cardiac sequelae. Acute hypocalcemia is more likely to manifest as neuromuscular (paresthesias, muscle cramps, tetany, and laryngeal spasm) and cardiovascular symptoms, whereas chronic hypocalcemia often presents as CNS (depression, anxiety, memory loss, confusion, hallucinations, and tonic-clonic seizures) and dermatologic symptoms (hair loss, grooved and brittle nails, and eczema). The hallmark sign of acute hypocalcemia is tetany caused by enhanced peripheral neuromuscular irritability. Tetany manifests as paresthesias around the mouth and in the extremities, muscle spasms and cramps, carpopedal (hands and feet) spasms, and rarely as... [Pg.956]

Before it can be unequivocally stated that apnea is caused by a prolonged peripheral neuromuscular block, the existence of such a block should be directly demonstrated by a peripheral nerve stimulator (B5). This is often not done, and therefore in many cases it is not possible to determine the true cause of the apnea, especially when there is some delay in following up the event. [Pg.26]

The pharmacology of insect central nervous system transmitter receptors and their associated modulatory sites and ion channels is less thoroughly known than that of the peripheral neuromuscular systems. This is in part due to the relative inaccessibility of the central... [Pg.31]

Peripheral neuromuscular paralysis (depolarising as part of the cholinergic syndrome)... [Pg.142]

Bradley, W. G., 1990, Critical review of gangliosides and thyrotropin releasing hormone in peripheral neuromuscular diseases. Muscle Nerve 13 833-842. [Pg.230]


See other pages where Peripheral neuromuscular is mentioned: [Pg.247]    [Pg.241]    [Pg.126]    [Pg.297]    [Pg.161]    [Pg.383]    [Pg.435]    [Pg.164]    [Pg.283]    [Pg.247]    [Pg.151]    [Pg.474]    [Pg.1601]    [Pg.891]    [Pg.57]    [Pg.104]    [Pg.148]    [Pg.131]    [Pg.117]    [Pg.154]    [Pg.246]    [Pg.568]    [Pg.41]    [Pg.42]    [Pg.418]   
See also in sourсe #XX -- [ Pg.42 ]




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Neuromuscular

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