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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1993-2-12
pubmed:abstractText
Certain results of in vitro studies raise the possibility that blockade of ATP-sensitive K+ channels by glibenclamide may induce vasoconstriction. Therefore, this substance might decrease portal pressure and hyperkinetic circulation in animals with portal hypertension. Thus, systemic and regional hemodynamics (radioactive microspheres) were measured before and 20 min after a bolus intravenous injection of glibenclamide (20 mg/kg) in conscious rats with portal vein stenosis. Blood pressure decreased significantly from 14.5 +/- 1.5 to 12.2 +/- 1.2 (mean +/- SE). Cardiac index significantly decreased by 24%, portal tributary blood flow by 31%, and hepatic artery blood flow by 35%. Systemic vascular resistance significantly increased by 38%, portal territory vascular resistance and hepatic artery vascular resistance by 61%, each, and renal vascular resistance by 17%. Arterial pressure, heart rate, and renal blood flow were unchanged. Moreover, glibenclamide blunted the vasodilating action of diazoxide (an ATP-sensitive K+ channel opener). These results show that in rats with extrahepatic portal hypertension the blockade of ATP-sensitive K+ channels by glibenclamide reduces portal pressure and hyperkinetic circulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0168-8278
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
215-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Blockade of ATP-sensitive K+ channels by glibenclamide reduces portal pressure and hyperkinetic circulation in portal hypertensive rats.
pubmed:affiliation
Laboratoire d'Hémodynamique Splanchnique, INSERM U-24, Hôpital Beaujon, Clichy, France.
pubmed:publicationType
Journal Article