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Pregled bibliografske jedinice broj: 727026

Časopis

Autori: McCallum, ruce J.; Boban, Nataša; Hogan, Quinn; Schmeling, William T.; Kampine, John P.; Bošnjak, Željko J.
Naslov: The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission
( The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission )
Izvornik: Anesthesia and analgesia (0003-2999) 87 (1998), 3; 503-510
Vrsta rada: članak
Ključne riječi: Acetylcholine/metabolism; Action Potentials/drug effects; Adrenergic alpha-2 Receptor Antagonists*; Ganglia; Sympathetic/drug effects*; Imidazoles/pharmacology*; Medetomidine; Norepinephrine/pharmacology; Stellate Ganglion/drug effects; Synaptic Transmission/drug effects*
( Acetylcholine/metabolism; Action Potentials/drug effects; Adrenergic alpha-2 Receptor Antagonists*; Ganglia; Sympathetic/drug effects*; Imidazoles/pharmacology*; Medetomidine; Norepinephrine/pharmacology; Stellate Ganglion/drug effects; Synaptic Transmission/drug effects* )
Sažetak:
Abstract Alpha2-adrenergic agonists produce analgesia and reduce hemodynamic stress through central and peripheral mechanisms, but the effect of adrenergic agonists on pre- and postganglionic sites has not yet been clarified. In this study, we examined the effects of dexmedetomidine (DMT), an alpha2-agonist, on neural conduction and neurotransmitter release in sympathetic ganglia. The stellate ganglia from 48 mongrel dogs were isolated, desheathed, and superfused with Krebs' solution. Compound action potentials were evoked, and chromatography was used to detect acetylcholine released by preganglionic stimulation in the presence or absence of DMT. To further elucidate the mechanism of alpha2 effects, DMT was applied in combination with the alpha2-antagonist atipamezole (AT) or the imidazoline antagonist idazoxan (ID). In other experiments, DMT was applied in the presence of exogenous nicotinic stimulation with 1, 1-dimethyl-4-phenylpiperazinium iodide or muscarinic stimulation with (+)cis-dioxolane. DMT dose-dependently inhibited synaptic transmission with a 50% effective dose of 71.6 (26.0-174.3) microM. Neurotransmitter release was reduced 25% by 70 microM DMT during low-frequency (0.4 Hz) stimulation, but this effect was abolished at higher frequency (5 Hz) stimulation. AT but not ID blocked the inhibitory action of DMT. DMT inhibited the excitatory postsynaptic response to exogenous muscarinic stimulation but not nicotinic stimulation. These results indicate that alpha2-receptor activation depresses ganglionic transmission through postsynaptic inhibition of muscarinic stimulation, although reduction of neurotransmitter release through a presynaptic autofeedback mechanism is also involved.
Izvorni jezik: eng
Rad je indeksiran u
bazama podataka:
Current Contents Connect (CCC)
MEDLINE
Scopus
SCI-EXP, SSCI i/ili A&HCI
Science Citation Index Expanded (SCI-EXP) (sastavni dio Web of Science Core Collectiona)
Kategorija: Znanstveni
Znanstvena područja:
Temeljne medicinske znanosti,Javno zdravstvo i zdravstvena zaštita
URL Internet adrese: http://journals.lww.com/anesthesia-analgesia/Abstract/1998/09000/The_Mechanism_of__alpha_2_Adrenergic_Inhibition_of.1.aspx
Broj citata:
Altmetric:
DOI: 10.1213/00000539-199809000-00001
URL cjelovitog teksta:
Google Scholar: The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission
Upisao u CROSBI: Nataša Boban (natasa.boban@mefst.hr), 4. Stu. 2014. u 15:07 sati



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