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neuromuscular blockade |
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blockade /block·ade/ (blok-ād´)
1. the blocking of the effect of a hormone or neurotransmitter at a cell-surface receptor by a pharmacologic antagonist bound to the receptor. 2. in histochemistry, a chemical reaction that modifies certain chemical groups and blocks a specific staining method. adrenergic blockade selective inhibition of the response to sympathetic impulses transmitted by epinephrine or norepinephrine at alpha or beta receptor sites of an effector organ or postganglionic adrenergic neuron. cholinergic blockade selective inhibition of cholinergic nerve impulses at autonomic ganglionic synapses, postganglionic parasympathetic effectors, or the neuromuscular junction. ganglionic blockade inhibition by drugs of nerve impulse transmission at autonomic ganglionic synapses. narcotic blockade inhibition of the euphoric effects of narcotic drugs by the use of other drugs, such as methadone, in the treatment of addiction. neuromuscular blockade a failure in neuromuscular transmission that can be induced pharmacologically or may result from pathological disturbances at the myoneural junction.
neuromuscular blockade, the inhibition of a muscular contraction activated by the nervous system, possibly resulting in muscle weakness or paralysis. blockade [blok-ād´] 1. in pharmacology, the blocking of the effect of a neurotransmitter or hormone by a drug. 2. in histochemistry, a chemical reaction that modifies certain chemical groups and blocks a specific staining method. adrenergic blockade selective inhibition of the response to sympathetic impulses transmitted by epinephrine or norepinephrine at alpha or beta receptor sites of an effector organ or postganglionic adrenergic neuron. See also adrenergic blocking agent. cholinergic blockade selective inhibition of cholinergic nerve impulses at autonomic ganglionic synapses, postganglionic parasympathetic effectors, or neuromuscular junctions. See also cholinergic blocking agent. ganglionic blockade inhibition by drugs of nerve impulse transmission at autonomic ganglionic synapses; see also ganglionic blocking agent. narcotic blockade inhibition of the euphoric effects of narcotic drugs by the use of other drugs, such as methadone, in the treatment of addiction. neuromuscular blockade a failure in neuromuscular transmission that can be induced pharmacologically or result from any of various disturbances at the myoneural junction. See also neuromuscular blocking agent. sympathetic blockade block of nerve impulse transmission between a preganglionic sympathetic fiber and the ganglion cell.
neuromuscular pertaining to nerve terminations in muscles. neuromuscular blockade deliberate paralysis of the motor end-plates; important in veterinary surgery for immobilization. It is effected by the use of competitive (non-depolarizing) agents such as d-tubocurarine, and depolarizing agents such as succinylcholine. neuromuscular blocking agents drugs capable of producing neuromuscular blockade (above). neuromuscular junction the point of junction of a nerve fiber with the muscle that it innervates. It includes an area of folded sarcolemma of the muscle fiber, and an axon terminal located in the folds and containing vesicles of the neurotransmitter acetylcholine. Called also myoneural junction. neuromuscular junction disease neuromuscular paralysis paralysis caused by malfunction at the neuromuscular junction, e.g. after administration of a neuromuscular blocking agent. The paralysis may be flaccid or spastic. phase-II neuromuscular block alteration of the end-plate threshold to depolarization by acetylcholine following prolonged use of a depolarization agent such as succinylcholine. neuromuscular spindle consists of muscle fiber, afferent and efferent nerve endings and connective tissue; maintains muscle tone via stretch reflex mediated through two neurons at spinal cord level. neuromuscular transmission
release of acetylcholine from the nerve ending and activation of the receptors in the muscle end-plate. neuromuscular blockade Neurology The partial or complete inhibition of motor activity at a neuromuscular junction Etiology 1. Reduction of post-synaptic receptors–eg, myasthenia gravis; 2. Defective acetylcholine release from storage
vesicles–eg, botulism, myasthenia, or Eaton-Lambert syndrome; 3. Competition for binding sites, either pharmacologic blockade–eg, neostigmine, edrophonium, or toxins–eg, organophosphate insecticides. See Neuromuscular junction. Want to thank TFD for its existence? Tell a friend about us, add a link to this page, add the site to iGoogle, or visit the webmaster's page for free fun content. |
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