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Titolo:
CLINICALLY RELEVANT CONCENTRATIONS OF BUPIVACAINE INHIBIT RAT AORTIC BARORECEPTORS
Autore:
CHANG KSK; YANG MY; ANDRESEN MC;
Indirizzi:
OREGON HLTH SCI UNIV,DEPT ANESTHESIOL,3181 SW SAM JACKSON PK RD PORTLAND OR 97201 OREGON HLTH SCI UNIV,DEPT PHYSIOL PORTLAND OR 97201 VET AFFAIRS MED CTR PORTLAND OR 00000
Titolo Testata:
Anesthesia and analgesia
fascicolo: 3, volume: 78, anno: 1994,
pagine: 501 - 506
SICI:
0003-2999(1994)78:3<501:CRCOBI>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMIDE LOCAL-ANESTHETICS; CENTRAL NERVOUS-SYSTEM; CARDIOVASCULAR TOXICITY; ARTERIAL BARORECEPTORS; MYOCARDIAL-INFARCTION; LIDOCAINE; HEART; ETIDOCAINE; INVITRO; DOGS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
K.S.K. Chang et al., "CLINICALLY RELEVANT CONCENTRATIONS OF BUPIVACAINE INHIBIT RAT AORTIC BARORECEPTORS", Anesthesia and analgesia, 78(3), 1994, pp. 501-506

Abstract

Bupivacaine is clinically associated with cardiovascular toxicity. Toexamine the possible role of drug actions at arterial baroreceptors, we studied discharge properties of baroreceptors in an in vitro aorticnerve-aortic arch preparation from rats. We measured single fiber discharge, pressure, and aortic diameter simultaneously during perfusion of the aortic arch with bupivacaine. Perfusion mean arterial pressure was held at 80 mm Hg. Only regularly discharging, presumably myelinated, baroreceptors were studied. To assess pressure threshold, thresholdfrequency, and maximum discharge rate, nerve activity was evoked by slow ramps of increasing pressure (<2 mm Hg/s) beginning at 20 mm Hg and ranging up to 150-170 mm Hg. Following replicate control measurements, test ramps were repeated in the presence of sodium nitroprusside (1mu M) and phentolamine (1 mu M) to eliminate potential smooth muscle and a(1)-adrenoceptor effects, respectively. Bupivacaine was then added to the perfusate in increasing concentrations from 0.1 to 50 mu M for 15 min to construct a full concentration-response curve at each level. Individual baroreceptors showed substantial depression of maximum discharge frequency and/or increases in pressure threshold at 1-5 mu M bupivacaine. In overall population averages (n = 7), 5-10 mu M bupivacaine clearly reduced maximum discharge and shifted the pressure threshold to higher values (P < 0.01). The net result was a general depression of discharge. Concentrations as low as 10 mu M bupivacaine completely blocked discharge in some baroreceptors. Inasmuch as the pressure-diameter relations were not changed, discharge relations plotted against diameter showed equivalent changes. Bupivacaine-free solution reversed the block in all cases. Our results suggest that arterial baroreceptors are substantially-to-completely blocked in the range of bupivacaine concentrations encountered during clinical crises and thus this action may contribute to the early cardiovascular sequelae observed.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 15:10:31