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Titolo:
Conduction block by clonidine is not mediated by alpha(2)-adrenergic receptors in rat sciatic nerve fibers
Autore:
Leem, JW; Choi, Y; Han, SM; Yoon, MJ; Sim, JY; Leem, SW;
Indirizzi:
Univ Ulsan, Coll Med, Dept Anesthesiol, Songpa Gu, Seoul, South Korea UnivUlsan Seoul South Korea Anesthesiol, Songpa Gu, Seoul, South Korea Yonsei Univ, Coll Med, Dept Physiol, Seoul, South Korea Yonsei Univ Seoul South Korea oll Med, Dept Physiol, Seoul, South Korea
Titolo Testata:
REGIONAL ANESTHESIA AND PAIN MEDICINE
fascicolo: 6, volume: 25, anno: 2000,
pagine: 620 - 625
SICI:
1098-7339(200011/12)25:6<620:CBBCIN>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRACHIAL-PLEXUS BLOCK; MEPIVACAINE PROLONGS; LIDOCAINE; EXCITATION; ANESTHESIA; ANALGESIA; AGONISTS; DURATION; NEURONS; INJURY;
Keywords:
clonidine; compound action potential; peripheral nerve block; adrenergic receptor; yohimbine; idazoxan;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Choi, Y Univ Ulsan, Coll Med, Dept Anesthesiol, Songpa Gu, 388-1 Poongnap Dong, Seoul, South Korea Univ Ulsan 388-1 Poongnap Dong Seoul South Koreaul, South Korea
Citazione:
J.W. Leem et al., "Conduction block by clonidine is not mediated by alpha(2)-adrenergic receptors in rat sciatic nerve fibers", REG ANES PA, 25(6), 2000, pp. 620-625

Abstract

Background and objectives: Clonidine. an alpha (2)-adrenergic agonist, hasbeen shown to prolong local anesthesia. It appears that clonidine by itself produces conduction block by acting on peripheral nerves. However, whether clonidine-induced conduction block is mediated through alpha (2)-adrenergic receptors remains unclear. The purpose of this study was to see if clonidine's nerve-blocking action was through alpha (2)-adrenergic receptors by examining clonidine's action in the presence of alpha (2)-adrenergic antagonists. Methods: The compound action potentials (CAPs) evoked by electrical stimuli were recorded from the isolated rat sciatic nerve in a recording chamber. Conduction block was examined by analyzing CAPs with regard to peak amplitude and time-to-peak in the presence of clonidine alone or clonidine plus alpha (2)-adrenergic antagonist yohimbine or idazoxan. Results: Both clonidine and yohimbine produced concentration-dependent, reversible, conduction block. Based on concentration-response relationships, the 50% of effective concentration (EC50) were estimated to he 1.61 +/- 0.51 mmol/L (mean +/- SD) for clonidine and 51.4 +/- 27.2 mu mol/L for yohimbine. A mixture of equal volumes of 2.07 mmol/L clonidine and 55.6 mu mol/L yohimbine produced conduction block to a level close to the mean value between conduction blocks induced by 2.07 mmol/L clonidine alone and 55.6 mu mol/L yohimbine alone. Addition of idazoxan, a more specific alpha (2)-adrenergic antagonist than yohimbine, to clonidine was without effect on clonidine-induced conduction block. Conclusions: The results indicated that the mixture of clonidine and yohimbine, in which either drug inhibited impulse conduction, produced conduction block in an additive manner, and that clonidine-induced conduction block was nor reversed by coapplication with a specific alpha (2)-adrenergic antagonist idazoxan, These data suggest that clonidine's effects likely depend on mechanisms not mediated by alpha (2)-adrenergic receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 09:35:07