Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-7-8
pubmed:abstractText
Increased tolerance to ischemia exhibited in chronically hypoxia immature rabbit hearts is associated with increased activation of ATP-sensitive potassium (KATP) channels. We determined whether exposure to hypoxia from birth alters the electrophysiological characteristics of Purkinje fibers obtained from rabbits (n = 12/group) which were raised in a normoxic (F O2 = 0.21) or hypoxic (F1O2 = 0.12) environment from birth to 9 days of age and the involvement of the KATP channel. The endocardial surface was exposed and impaled with microelectrodes to record action potential characteristics from Purkinje fibers under control conditions and following exposure to glibenclamide (3 microM). Action potential durations (APD)90 in Purkinje fibers were significantly shorter in hypoxic hearts compared with normoxic controls (110 +/- 5 ms v 121 +/- 4 ms). Glibenclamide increased APD90 in hypoxic hearts (120 +/- 4 ms) to values similar to those observed in normoxic controls (121 +/- 4 ms). Glibenclamide had no effect on APD90 in normoxic hearts. Maximum diastolic potential was more negative in hypoxic hearts and this effect was attenuated by glibenclamide. We conclude that chronic myocardial hypoxia results in a shorter APD as compared with normoxic controls by enhanced activation of KATP channels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
845-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
KATP channel activation in a rabbit model of chronic myocardial hypoxia.
pubmed:affiliation
Department of Pharmacology, Medical College of Wisconsin, Milwaukee 53226, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't