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Neuromuscular ability

Postnatally, offspring were tested for olfaction, neuromuscular ability, exploratory and circadian activity, aversive and appetitive learning." There was evidence of impaired neuromuscular ability." Offspring from dams exposed on days 7-13 were poorer than controls in ascent of a wire mesh screen during the second week of life and were poorer than controls on a rotorod test on one of the 3 days tested in the fourth week of life." Offspring from dams exposed on days 14-20 performed less well in ascent of a wire mesh screen. [Pg.1337]

These materials are fourth generation chemical warfare agents. They contain one or more quaternary amine centers that increase the ability of the agent to penetrate into neuromuscular junctions. They are relatively simple to synthesize although the starting materials are not commonly available. Because they produce negligible vapor, they are somewhat difficult to deliver in a manner that will produce immediate casualties. [Pg.105]

Propofol is primarily a hypnotic drug with substantial cardiorespiratory depressant actions and with no ability to produce neuromuscular blockade. While propofol lacks analgesic properties, its use permits lower doses of opioids. Likewise, less propofol is required for adequate hypnosis when it is administered with opioids. Thus, it is said that propofol and opioids interact synergistically. [Pg.296]

Holmes and Robins reported that 2-PAM I overcame neuromuscular blockade induced by DFP, TEPP, or sarin, but this could be demonstrated with the Isolated phrenic nerve-diaphragm preparation from the rat only after washing away excess OP compound. Intravenous injection of 2-PAM I overcame slowly neuromuscular blockade induced by OP compounds. The oxime, they found, also had a direct toxic action on muscle, reducing the ability of muscle to shorten and decreasing the ability of muscle fibers to conduct impulses. The same investigators reported that V (intraperltoneally at 150 mg/kg) had little, if any, effect on a sarin-induced blockade of neuromuscular transmission. [Pg.281]

Neuromuscular blockade produced by succinylcholine and mivacurium can be prolonged in patients with a genetically abnormal variant of plasma cholinesterase. The dibucaine number is a measure of the ability of a patient to metabolize succinylcholine and can be used to identify at-risk patients. Under standardized test conditions, dibucaine inhibits the normal enzyme by 80% and the abnormal enzyme by only 20%. Many genetic variants of plasma cholinesterase have been identified, although the dibucaine-related variants are the most important. Given the rarity of these genetic variants, plasma cholinesterase testing is not a routine clinical procedure. [Pg.582]

Levamisole acts as a ganglion-stimulating compound and induces a neuromuscular inhibition of the depolarizing type. However, it is possible that its ability to act as an immune stimulant may also contribute to its activity. [Pg.203]

When the calcium ion concentration is lowered in the fluids bathing nerve axons ifluids which are in very rapid equilibrium with the blood plasma) the electrical resistance ol the axon membrane is lowered, there is increased movement of sodium ions to ihe inside, and the ability ol ihe nerve to return io iis normal siale fallowing a discharge is slowed. Thus, on the one hand, there is hyperexcitabilily. Bui. the ability lor synaptic transmission is inhihited because the rate of acetylcholine liberation is a function ot ihe calcium ion concentration. The neuromuscular junction is... [Pg.271]

Release. Certain drugs will increase synaptic activity by directly increasing the release of neurotransmitter from the presynaptic terminal. Amphetamines appear to exert their effects on the CNS primarily by increasing the presynaptic release of catecholamine neurotransmitters (e.g., norepinephrine). Conversely, other compounds may inhibit the synapse by directly decreasing the amount of transmitter released during each action potential. An example is botulinum toxin (Botox), which can be used as a skeletal muscle relaxant because of its ability to impair the release of acetylcholine from the skeletal neuromuscular junction (see Chapter 13). [Pg.61]

Curare was first brought to the attention of Queen Elizabeth of England by Sir Walter Raleigh. The remarkable ability of the drug to induce paralysis of the muscles led to its early use by Claude Bernard, Kolliker, Langley, and subsequent physiologists to study the mechanism of neuromuscular activity. However, the uncertain supplies of the drug, its variability, and the effects of its contaminants prevented its therapeutic application. [Pg.287]

Some strains have difficulties balancing on an aluminum rod, and a more textured surface (e.g., wood) may help stabilize the animal. Increasing the diameter of the rod is another possible solution. If mice continue to struggle with balance or motor abilities, assess motor and vestibular functions separately as these behaviors may be due to a neuromuscular or motor coordination problem unrelated to vestibular deficits or anxiety. [Pg.317]

This is an autoimmune disease in which there is muscle weakness without any change in the individual s ability to feel things. In myasthenia gravis antibodies block, alter or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction from occurring. Hence with fewer receptor sites available the muscles receive fewer nerve signals. [Pg.142]

Fig. 3. Effects of 5 days of intensive oral dosing with vitamin E (200 IU/day) plus selenium (50 pg/day) on early degeneration of cat soleus motor nerve terminals at 48 hours after motor axon section. On the left is a comparison of the nerve-evoked contractile tension in the 48-hour degenerating soleus nerve-muscle preparations to that observed in the contralateral normal preparations. In the untreated animals, about 50% of the motor nerve fibers have ceased to excite their innervated muscle fibers. In contrast, antioxidant pretreatment resulted in a significant preservation of neuromuscular function. Similarly, on the right, a comparison of the ability of the motor nerves to maintain repetitive transmission at a high frequency (100 Hz) for a 10-second period also shows a better preservation of this neuromuscular parameter in the antioxidant pretreated animals. Fig. 3. Effects of 5 days of intensive oral dosing with vitamin E (200 IU/day) plus selenium (50 pg/day) on early degeneration of cat soleus motor nerve terminals at 48 hours after motor axon section. On the left is a comparison of the nerve-evoked contractile tension in the 48-hour degenerating soleus nerve-muscle preparations to that observed in the contralateral normal preparations. In the untreated animals, about 50% of the motor nerve fibers have ceased to excite their innervated muscle fibers. In contrast, antioxidant pretreatment resulted in a significant preservation of neuromuscular function. Similarly, on the right, a comparison of the ability of the motor nerves to maintain repetitive transmission at a high frequency (100 Hz) for a 10-second period also shows a better preservation of this neuromuscular parameter in the antioxidant pretreated animals.

See other pages where Neuromuscular ability is mentioned: [Pg.349]    [Pg.64]    [Pg.349]    [Pg.64]    [Pg.798]    [Pg.322]    [Pg.55]    [Pg.188]    [Pg.3]    [Pg.4]    [Pg.1072]    [Pg.104]    [Pg.276]    [Pg.124]    [Pg.752]    [Pg.295]    [Pg.179]    [Pg.281]    [Pg.284]    [Pg.293]    [Pg.295]    [Pg.1072]    [Pg.583]    [Pg.594]    [Pg.101]    [Pg.159]    [Pg.317]    [Pg.402]    [Pg.582]    [Pg.631]    [Pg.381]    [Pg.103]    [Pg.61]    [Pg.186]    [Pg.798]    [Pg.192]    [Pg.415]   
See also in sourсe #XX -- [ Pg.551 ]




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Neuromuscular

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