Differential Sensitivities of Mammalian Nerve Fibers to Local Anesthetic Agents

Gissen, Aaron J.; Covino, Benjamín G.; Gregus, J.

doi:10.1097/00000542-198012000-00006

Cited by 174 publications

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“…Lidocaine has been demonstrated previously to block not only sensory, but also non-sensory (motor and sympathetic) nerve fibers. 13,24,30,45 It has also been demonstrated in isolated rat sciatic nerve that perineural capsaicin application potentiates the effect of subsequent lidocaine application. 41 Since no evidence has so far been presented for the involvement of fibers other than sensory and sympathetic nerve fibers in neurogenic skin vasomotor control, the effect of lidocaine application to capsaicin-pretreated nerves on SBF abnormalities can most likely be attributed to blockade of impulse propagation of sympathetic nerve fibers.…”

Section: Experimental Protocol Skin Blood Flow Measurementsmentioning

confidence: 99%

Skin blood flow disturbances in the contralateral limb in a peripheral mononeuropathy in the rat

et al. 1996

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Section: Experimental Protocol Skin Blood Flow Measurementsmentioning

confidence: 99%

Skin blood flow disturbances in the contralateral limb in a peripheral mononeuropathy in the rat

et al. 1996

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“…Indeed, studies have shown that cocaine reduces cerebral blood flow (CBF) and blood volume in human subjects and in laboratory animals (Volkow et al, 1988;Pearlson et al, 1993;Wallace et al, 1996;Schmidt et al, 2006). Cocaine has multiple pharmacological targets including blockade of the dopamine, serotonin, and norepinephrine transporters (Ritz et al, 1987) that give it its sympathomimetic effects and blockade of sodium channels, which gives it its local anesthetic actions (Gissen et al, 1980). Cocaine-induced reductions in CBF could reflect (1) direct vasoconstrictive effects elicited via increases in intracellular calcium ([Ca 2ϩ ] i ) in vascular smooth muscle (Zhang et al, 1996), (2) indirect vasconstriction secondary to increases of sympathomimetic amines, or (3) an indirect consequence of reduced neural activity and metabolic demand attributable to blockade of sodium channels.…”

Section: Introductionmentioning

confidence: 99%

Cocaine Increases the Intracellular Calcium Concentration in Brain Independently of Its Cerebrovascular Effects

Du¹,

Yu²,

Volkow³

et al. 2006

J. Neurosci.

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Cocaine abuse increases the risk of life-threatening neurological complications such as strokes and seizures. Although the vasoconstricting properties of cocaine underlie its cerebrovascular effects, the mechanisms underlying its neurotoxicity remain incompletely understood. ] i in the brain. The effects of cocaine were compared with those of methylphenidate, which has similar catecholaminergic effects as cocaine (except for serotonin increases) but no local anesthetic properties, and of lidocaine, which has similar local anesthetic effects as cocaine but is devoid of catecholaminergic actions. To control for the hemodynamic effects of cocaine, we assessed the effects of cocaine in animals in which normal blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of transient hypotension (mimicking that induced by cocaine). We show that cocaine induced significant increases (ϳ10 -15%) in [Ca 2ϩ ] i that were independent of its hemodynamic effects and of the anesthetic used (isofluorance or ␣-chloralose).

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“…CST studies have not yet been used to assess dose-dependent nerve blockade induced by local anesthesia in animal models of spinal anesthesia. Although anesthesiologists attribute differential nerve fiber blockade at reversible neural block to differences in nerve fiber diameter, conduction velocity, or surrounding myelination, the real causes remain unclear (Gasser and Erlanger, 1929;Gissen et al, 1980;Fink, 1989). Irreversible neural injury caused by high concentrations of local anesthetic in spinal anesthesia has become a serious problem over the past 15 years, and the underlying mechanisms are likewise unknown (Rigler et al, 1991;Drasner et al, 1994;Sakura et al, 1995a,b).…”

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confidence: 99%

Quantitative and Fiber-Selective Evaluation of Dose-Dependent Nerve Blockade by Intrathecal Lidocaine in Rats

Oda¹,

Kitagawa²,

Yang³

et al. 2004

J Pharmacol Exp Ther

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We investigated whether cutaneous stimulus threshold (CST), as determined using a Neurometer, could be used for quantitative and differential nerve evaluation of reversible and irreversible nerve block following intrathecal lidocaine administration in rats. Rats with intrathecal catheters were randomly assigned to one of five groups (saline or 2, 5, 10, or 20% lidocaine). Prior to and 4 days after drug administration, CST was determined at 5, 250, and 2000 Hz. In the 2% lidocaine group, CST from end of lidocaine infusion to recovery from anesthesia was also monitored. Skin-clamp testing and gait observation were performed for comparison with CST findings. Behavioral examinations revealed persistent sensory or motor impairment lasting 4 days in groups receiving Ն5% lidocaine but not in the saline and 2% lidocaine groups. With 2% lidocaine, return to baseline CSTs at 5 and 250 Hz was delayed compared with thresholds at 2000 Hz. Although CSTs in the 5% group at 5 and 250 Hz increased significantly, thresholds at 2000 Hz did not differ from those in rats administered saline. CSTs with Ն10% lidocaine displayed no differences between frequencies. At each frequency, CSTs for rats with Ն5% lidocaine increased in a clearly concentration-dependent manner. These results suggest that CST testing enables evaluation of the different nerve functions for A␤, A␦, and C fibers in rats for lidocaine concentrations Յ5% and allows quantitative assessment of persistent neurological deficit induced by lidocaine in rats.

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Differential Sensitivities of Mammalian Nerve Fibers to Local Anesthetic Agents

Cited by 174 publications

References 0 publications

Skin blood flow disturbances in the contralateral limb in a peripheral mononeuropathy in the rat

Skin blood flow disturbances in the contralateral limb in a peripheral mononeuropathy in the rat

Cocaine Increases the Intracellular Calcium Concentration in Brain Independently of Its Cerebrovascular Effects

Quantitative and Fiber-Selective Evaluation of Dose-Dependent Nerve Blockade by Intrathecal Lidocaine in Rats

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