Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1990-5-14
pubmed:abstractText
The cardiotoxic effect of the beta-adrenergic agonist isoproterenol was studied in cultured neonatal rat myocytes. A progressive increase in irreversible cell injury as determined by leakage of the cytoplasmic enzyme alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) from the cells was noted at concentrations above 2.5 x 10(-4) M isoproterenol (exposure time 6 h). The isoproterenol-induced cell damage was reduced or prevented by several free radical scavengers: the application of Trolox C, a water-soluble vitamin E analogue, ICRF-159, a chelator of divalent cations, ascorbic acid, a potent antioxidant, as well as the enzymatic free radical scavengers superoxide dismutase and catalase reduced alpha-HBDH release. This study corroborates the hypothesis that oxidation products of isoproterenol, especially the formation of oxygen- and/or oxygen-derived free radicals, are responsible for the cytotoxicity observed after prolonged exposure to isoproterenol. In contrast to isoproterenol, exposure to 5 x 10(-4) M fenoterol, another beta-adrenergic agonist which is not oxidized, does not impair the viability of the myocytes. Moreover, application of the beta-blocker propranolol (10(-4) M, 10(-5)M) in combination with 5 x 10(-4) M isoproterenol does not prevent alpha-HBDH release. These findings suggest that isoproterenol-induced cardiotoxicity is not the result of excessive beta-adrenoceptor activation, but is mediated by the formation of free radicals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1285-91
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Isoproterenol-induced cytotoxicity in neonatal rat heart cell cultures is mediated by free radical formation.
pubmed:affiliation
Department of Cardiology, University Hospital, Leiden, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't