Mitochondrial big conductance KCa channel and cardioprotection in infant rabbit heart. J Cardiovasc Pharmacol 2007 Nov;50(5):497-502
Date
11/22/2007Pubmed ID
18030058DOI
10.1097/FJC.0b013e318137991dScopus ID
2-s2.0-36349013696 (requires institutional sign-in at Scopus site) 33 CitationsAbstract
Chronic hypoxia increases resistance to myocardial ischemia in infants. Activation of the mitochondrial big conductance Ca(2+) -sensitive K channel (mitoBKCa) has been shown to be protective in adult hearts; however, its role in infant hearts is unknown. Hearts from normoxic or hypoxic infant rabbits were perfused with a mitoKCa opener, NS1619, or blocker Paxilline before ischemia and reperfusion. Hypoxic hearts were more resistant to ischemia than normoxic hearts as manifested by a reduction in infarct size (9 +/- 5% versus 14 +/- 5%) and an increase in recovery of left ventricular developed pressure (LVDP) (69 +/- 7% versus 51 +/- 2%). NS1619 decreased infarct size in normoxic hearts from 14 +/- 5% to 10 +/- 5% and increased recovery of LVDP from 51 +/- 2% to 65 +/- 4%, but it had no effect on hypoxic hearts. Paxilline did not affect normoxic or hypoxic hearts. Activation of mitoBKCa protects normoxic infant rabbit hearts; however, cardioprotection by chronic hypoxia in infant rabbits does not appear involve mitoBKCa.
Author List
Shi Y, Jiang MT, Su J, Hutchins W, Konorev E, Baker JEAuthor
John E. Baker PhD Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAnimals, Newborn
Benzimidazoles
Coronary Circulation
Heart
Heart Rate
Hypoxia
Indoles
Ischemic Preconditioning, Myocardial
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
Large-Conductance Calcium-Activated Potassium Channels
Mitochondria
Myocardial Infarction
Myocardial Reperfusion Injury
Myocardium
Perfusion
Potassium Channel Blockers
Potassium Channels
Rabbits
Ventricular Function
