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Conduction velocity

Conductivity. Conductivity is an electrical property of excitable tissue which ensures that if one area of a membrane is excited to full activity, that area excites adjacent areas. Conduction of an impulse varies direcdy with the rate of development of phase 0 and the ampHtude of the action potential. Phase 0 is faster, and ampHtude of the action potential is greater, the more negative the transmembrane potential at the time of initiation of the impulse. Conduction velocity is faster when phase 0 is fast. [Pg.111]

The Class I agents decrease excitability, slow conduction velocity, inhibit diastoHc depolarization (decrease automaticity), and prolong the refractory period of cardiac tissues (1,2). These agents have anticholinergic effects that may contribute to the observed electrophysiologic effects. Heart rates may become faster by increasing phase 4 diastoHc depolarization in SA and AV nodal cells. This results from inhibition of the action of vagaHy released acetylcholine [S1-84-3] which, allows sympathetically released norepinephrine [51-41-2] (NE) to act on these stmctures (1,2). [Pg.112]

Glass IB Antiarrhythmic Agents. Class IB antiarrhythmic agents produce less inhibition of the inward sodium current than Class lA agents. In normal myocardial tissue, phase 0 may be unaffected or minimally depressed. However, in ischemic or infarcted tissue, phase 0 is depressed. Myocardial tissue exposed to Class IB agents exhibits decreased automaticity, shortened action potential duration, ie, shortened repolarization, and shortened refractory period. Excitability of the myocardium is not affected and conduction velocity is increased or not modified. The refractory period is shortened less than its action potential duration, thus the ratio of refractory period to action potential duration is increased by these agents. The net effect is increased refractoriness. The PR and QT intervals of the ECG are shortened and the QRS interval is unchanged (1,2). [Pg.113]

ALA, ALA-D = aminolevulinic acid dehydrase NCV = nerve conduction velocity... [Pg.370]

Mechanisms of Cardiotoxicity Chemical compounds often affect the cardiac conducting system and thereby change cardiac rhythm and force of contraction. These effects are seen as alterations in the heart rate, conduction velocity of impulses within the heart, and contractivity. For example, alterations of pH and changes in ionic balance affect these cardiac functions. In principle, cardiac toxicity can be expressed in three different ways (1) pharmacological actions become amplified in an nonphysiological way (2) reactive metabolites of chemical compounds react covalently with vital macromolecules... [Pg.296]

Decreases the conduction velocity through the atrioventricular (AV) and sinoatrial (SA) nodes in the heart... [Pg.358]

Action potentials, self-propagating. Action potentials of smooth muscle differ from the typical nerve action potential in at least three ways. First, the depolarization phases of nearly all smooth muscle action potentials are due to an increase in calcium rather than sodium conductance. Consequently, the rates of rise of smooth action potentials are slow, and the durations are long relative to most neural action potentials. Second, smooth muscle action potentials arise from membrane that is autonomously active and tonically modulated by autonomic neurotransmitters. Therefore, conduction velocities and action potential shapes are labile. Finally, smooth muscle action potentials spread along bundles of myocytes which are interconnected in three dimensions. Therefore the actual spatial patterns of spreading of the action potential vary. [Pg.193]

The clinical neuroscience community was quick to pick up on the importance of this discovery and Barker s Transcranial Magnetic Stimulation (TMS) was soon widely used to measure nerve conduction velocities in clinical and surgical settings. However, it is not in the clinical domain that magnetic stimulation provides the most excitement magnetic stimulation is a tool with which to discover new facts about brain function and it has already delivered in many areas. [Pg.177]

Triebig G, Reichenbach TH, Flugel KA. 1978. [Biochemical examinations and measurements of the conduction velocity in persons chronically exposed to trichloroethylene.] Int Arch Occup Environ Health 42 31-40. (German)... [Pg.293]

Primary afferent fibre type Mean diameter (gm) Myelination Mean conduction velocity (m/s)... [Pg.455]

The afferent fibres differ in their conduction velocity and degree of myelination, and can be distinguished by their diameter. The large diameter A S-fibres are myelinated by Schwann cells and hence have a fast conduction velocity. This group of nerve fibres innervates receptors in the dermis and is involved in the transmission of low-threshold, non-noxious information, such as touch. The A5-fibre is less densely myelinated and conveys both non-noxious and noxious sensory information. The unmyelinated C-fibre conveys high-threshold noxious inputs and has the slowest conduction velocity of all three fibre types. [Pg.455]

Subcllnlcal effects clinical laboratory test alteration (liver function, nerve conduction velocity), mutagenicity testing, cytogenetic testing Requires estimation of eventual likelihood of clinical disease predicted by subcllnlcal abnormalities ... [Pg.9]

Inhibitors of AR have been demonstrated to prevent a wide variety of biochemical, functional and structural alterations in animal models of diabetes. Early studies demonstrated arrest of both early cataract development and nerve conduction velocity. At least 30 clinical trials of AR inhibitors have been published involving nearly 1000 patients in total. However, there is little impressive data of their efficacy up to now but, rather than undermine the hypothesis linking excess polyol pathway activity to diabetic complications, it may reflect methodological difficulties and trial design errors. [Pg.191]

Type Drug Automaticity Conduction velocity Refractory period Blockade... [Pg.38]

Describe the modified Vaughan-Williams classification of antiarrhythmic drugs, and compare and contrast the effects of available antiarrhythmic drugs on ventricular conduction velocity, refractory period, automaticity, and inhibition of specific myocardial ion channels. [Pg.107]

Caffeine and theophylline increase the conduction velocity in the heart. [Pg.234]

The intermediate-duration effects of hydrogen sulfide on neurological function were examined by the measurement of motor and sensory nerve conduction velocities of the tail nerve or morphology of the sciatic nerve (Gagnaire et al. 1986). Male Sprague-Dawley rats were exposed to 0 or 50 ppm hydrogen sulfide for 5 days a week, for 25 weeks. The study authors did not report the duration of exposure to hydrogen sulfide per day. No neurotoxic effects were observed in the rats. [Pg.68]

NS (occup) Neurological Peripheral nerve function in adults decreased nerve conduction velocity 30- 70 Araki et al. 1980 Chia et al. 1996 Muijser et al. 1987 Rosen et al. 1983 Seppalainen et al. 1983 Triebig et al. 1984... [Pg.42]

NS (general population) Neurological Peripheral neuropathy and reduced conduction velocity in children 20-30 Erenberg et al. 1974 Landringan et al. 1976 Schwartz et al. 1988 Seto and Freeman 1964... [Pg.44]

There is suggestive evidence indicating that the changes in NCV associated with lead exposure may be transient. Muijser et al. (1987) investigated the effects of a 5-month exposure to lead during the demolition of a steel structure coated with lead-based paints. The motor and sensory nerve conduction velocities were measured in the median and ulnar nerves of eight exposed workers and compared with unexposed referents as well as themselves at 3 and 15 months after the termination of exposure. The mean PbB levels in the exposed workers were 82.5 18.9 pg/dL at the termination of exposure,... [Pg.89]

Anderson RJ. 1987. Peripheral nerve conduction velocities and excitability. In Lowndes HE, ed. Electrophysiology in neurotoxicology, Vol. 11. Piscataway, NJ Department of Pharmacology and Toxicology, Rutgers 51-69. [Pg.487]

Araki S, Honma T, Yanagihara S, et al. 1980. Recovery of slowed nerve conduction velocity in lead-exposed workers. Int Arch Occup Environ Health 46 151-157. [Pg.488]


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See also in sourсe #XX -- [ Pg.56 ]




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