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Titolo:
Effect of tamsulosin hydrochloride on sympathetic hyperactivity in amyotrophic lateral sclerosis
Autore:
Ohno, T; Shimizu, T; Kato, S; Hayashi, H; Hirai, S;
Indirizzi:
Tokyo Metropolitan Neurol Hosp, Dept Neurol, Fuchu, Tokyo 1830042, Japan Tokyo Metropolitan Neurol Hosp Fuchu Tokyo Japan 1830042 o 1830042, Japan
Titolo Testata:
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
fascicolo: 1-2, volume: 88, anno: 2001,
pagine: 94 - 98
SICI:
1566-0702(20010412)88:1-2<94:EOTHOS>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA-ADRENOCEPTORS; BLOOD-PRESSURE; RAT; ALPHA(1)-ADRENOCEPTOR; NOREPINEPHRINE; SUBTYPES; SYSTEM; PLASMA;
Keywords:
amyotrophic lateral sclerosis; sympathetic hyperactivity; tamsulosin hydrochloride;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Shimizu, T Tokyo Metropolitan Neurol Hosp, Dept Neurol, 2-6-1 Musashidai, Fuchu, Tokyo 1830042, Japan Tokyo Metropolitan Neurol Hosp 2-6-1 MusashidaiFuchu Tokyo Japan 1830042
Citazione:
T. Ohno et al., "Effect of tamsulosin hydrochloride on sympathetic hyperactivity in amyotrophic lateral sclerosis", AUTON NEURO, 88(1-2), 2001, pp. 94-98

Abstract

We assessed subclinical sympathetic hyperactivity in amyotrophic lateral sclerosis (ALS) patients, which might be followed by an autonomic spell leading to circulatory collapse, or sudden death as the disease progresses, andinvestigated the effect of tamsulosin hydrochloride (TSHC) on sympathetic hyperactivity. We measured the plasma norepinephrine (NE) concentrations of41 ALS patients and 10 normal controls. TSHC, a selective alpha 1 blocker,was then administered to 10 ALS patients who had high plasma NE and to the10 normal controls. Subsequent plasma NE change was evaluated for the possible alleviating effect of TSHC on subclinical sympathetic hyperactivity inALS. Plasma NE was high in 20 of the ALS patients (48.8%), but had no relation to respiratory problems, which supports the previous speculation that plasma NE increases in ALS are not secondary to respiratory deficit, but reflect the primary pathomechanism of the disease. ALS patients showed a marked decrease in the NE concentration after TSHC administration, whereas there was no change in the controls. In conclusion. TSHC may be useful for suppressing central sympathetic hyperactivity. presumably the primary pathomechanism in ALS, and for preventing autonomic spells during the advanced stageof the disease. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 02:07:23