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Reflex excitability

Anhalonine produces increased reflex excitability in the frog after a phase of paresis (Heffter, 1898). The symptoms in the rabbit are analogous, but the transitory paresis is less marked. The lethal dose of the hydrochloride for rabbits is 0-16-0-2 gm. per kilo, body weight. [Pg.160]

Codeine (morphine methyl ether) resembles morphine in its general effect, but is less toxic and its depressant action less marked and less prolonged, whilst its stimulating action involves not only the spinal cord, but also the lower parts of the brain. In small doses in man it induces sleep, which is not so deep as that caused by morphine, and in large doses it causes restlessness and increased reflex excitability rather than sleep. The respiration is slowed less than by morphine (cf. table, p. 261). Cases of addiction for codeine can occur but according to Wolff they are rare. The best known ethers of morphine are ethylmorphine and benzyl-morphine [cf., table, p. 261), both used to replace morphine or codeine for special purposes. [Pg.265]

The simpler substance apoharmine according to Flury causes increased reflex excitability in the dog. In the frog it produces a like effect which with larger doses goes on to tetanus. Esterification of harmol with methylcarbamic acid induces affinities with the physostigmine type of drug. ... [Pg.497]

The lethal oral dose in humans is probably around 100, but doses as low as 16 mg have reportedly been fatal whereas doses of 2 000 mg have been survived. After ingestion, effects usually occur within 10-30 minutes and include stiffness of the face and neck muscles and increased reflex excitability. Strychnine acts by altering nerve impulses in the spinal cord, resulting in a decreased threshold for stimulation, and, hence, a hyperexcitable state. Any sensory stimulus may produce a violent motor response that, in the early stages of intoxication, tends to be a coordinated extensor thrust and, in later stages, may be a tetanic convulsion with opisthotonos anoxia and cyanosis develop rapidly. Between convulsions, muscular relaxation is complete, breathing is resumed, and cyanosis lessens. Because sensation is unaffected, the convulsions are painful and lead to overwhelming fear. As many as 10 convulsions separated by intervals of 10-15 minutes may be experienced, but death often occurs after the second to fifth convulsion, and even the first convulsion may be fatal if sustained death is commonly due to asphyxia.If recovery occurs, it is remarkably prompt and complete despite the violence of the illness muscle soreness may persist for a number of days. ... [Pg.640]

The exactly opposite effects of drugs and dreams on pupillary aperture and reflex excitability are important examples of informative differences between the two states. REM sleep is off-line—that is, the brain is dissociated from inputs and outputs—precisely because access of afferent stimuli to the CNS is blocked (e.g., pupillary myosis), as is access of internally generated motor commands to the peripheral muscles (e.g., inhibited deep tendon reflexes). Were this not the case, REM sleep would be waking (or a hybrid state even more like drug psychosis). And if the converse were... [Pg.263]

In lower mammals, scopolamine reduces the excitability of the motor areas as tested by electric shocks, and the reflex excitability in the frog is not increased as by atropine. Scopolamine appears to be excreted or destroyed in the tissues much more rapidly than atropine, for its effects last a shorter time. [Pg.205]

Briellmann RS, Rosier KM, Hess CW (1996). Blink reflex excitability is abnormal in patients with periodic leg movements in sleep. Mov Disord 11 710—714... [Pg.77]

At near lethal concentrations of -butylamine administered orally, rats and rabbits exhibited increased reflex excitability, increased pulse and respiration, dyspnea, convulsions, cyanosis, and coma. The LD50 in rats was reported to be 147 mg kg for s-butylamine and 78 mg kg for t-butylamine. The oral LD50 in rats was reported to be 366 mg kg for -butylamine, with death due to pulmonary edema. Prior to death, the rats exhibited sedation, ataxia, nasal discharge, gasping, salivation, and convulsions. [Pg.362]

HoAvever, Schweitzer and Wright (8) claim different results, and state that atropine decreases the inhibitory action of acetylcholine on the respiratory center. Gesell and Hansen (127) admit that atropine abolishes all respiratory modifications due to eserine or acetylcholine. However, Hey-mans and coworkers (128) observed that atropine, acting on the central nervous system, does not affect the direct or reflex excitability of the respiratory center or the parasympathetic cardio-inhibitory center. [Pg.126]

Widdicombe JG (1954a) Receptors in the trachea and bronchi of the cat. J Physiol 123 71-104 Widdicombe JG (1954b) Respiratory reflexes excited by inflation of the lungs. J Physiol 123 105-115... [Pg.46]

Anhalonine was examined by Heffter (47) 5-10 mg., when injected in the frog, produced an increase in the reflex excitability after a phase of paresis. In the rabbit similar symptoms are observed but general h3rper-excitability predominantes. [Pg.19]

Its pharmacological action is very similar to that of the isoquinoline bases obtained from Anhalonium lewinii (27, 48). The lethal dose in the frog is 3-4 mg. the injection of 2-3 mg. of hydrochloride produces increased reflex excitability and convulsions larger doses cause paresis. Carnegine provokes convulsions also in warm-blooded animals. [Pg.20]

Documented effects The alkaloid protopine (fumarine) caused narcosis in amphibians and, in mammals, caused paralysis of sensory nerve endings and increased reflex excitability. The alkaloid slightly increased the effects of analeptics and induced catalepsy (Chen-Gu 1957 Cheney 1963). In acute experiments with animals under narcosis, reduced heart rate and increased heartbeat amplitude occurred and, for a short time, decreased blood pressure was observed. Protopine has antiarrhythmic action with better effects than novocainamide and quinidine (Sadritdinov and Kurmukov 1980). In a screen to determine effects on platelet aggregation, extracts of this species showed complete inhibition of aggregation. This result was found to be caused by protopine (Sener 1994). Extracts of the dried plant displayed high rates of inhibition against the enzymes acetylcholinesterase and butyrylcholinesterase, which are associated with Alzheimer s disease (Orhan et al. 2004). [Pg.118]

Symptoms of Exposure Stiff neck, muscle fasiculation, restlessness, apprehension, acuity of perception, reflex excitability, cyanosis, tetanic convulsions, opisthotonos. [Pg.203]

Reciprocal innervation. When a stretch reflex excites one muscle, it simultaneously inhibits the antagonist muscle. Reciprocal... [Pg.49]

Reciprocal inhibition. This is used in active myofascial techniques with or without resistance. When a stretch reflex stimulates one muscle, it simultaneously inhibits the antagonist muscle e.g., if the stretch reflex excites the biceps, reciprocal inhibition inhibits the triceps. [Pg.81]

Muscle contraction dynamics include the mechanical properties of muscle tissues and tendons, which are expressed as force-length and force-velocity relations. The activation dynamics include the voluntary and nonvoluntary (reflex) excitation signal and motor unit recruitment level in the muscle. It is well known that regardless of fatigue, the generated torque in each joint is dependent on muscle activation levels (MALs) and joint angle when in a stationary position. This was first observed by Tnman et al. [Pg.157]

Reduced reflex excitability of both flexors and extensors (Wand et al., 1977)... [Pg.593]


See other pages where Reflex excitability is mentioned: [Pg.273]    [Pg.305]    [Pg.496]    [Pg.264]    [Pg.456]    [Pg.464]    [Pg.227]    [Pg.498]    [Pg.530]    [Pg.531]    [Pg.264]    [Pg.526]    [Pg.644]    [Pg.52]    [Pg.286]    [Pg.298]    [Pg.144]    [Pg.413]    [Pg.260]    [Pg.561]    [Pg.577]    [Pg.50]    [Pg.631]    [Pg.719]   
See also in sourсe #XX -- [ Pg.118 ]




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