Sarcolemmal and mitochondrial K(atp)channels mediate cardioprotection in chronically hypoxic hearts. J Mol Cell Cardiol 2001 May;33(5):1041-5
Date
05/10/2001Pubmed ID
11343425DOI
10.1006/jmcc.2001.1362Scopus ID
2-s2.0-0034971965 31 CitationsAbstract
X. Kong, J. S. Tweddell, G. J. Gross and J. E. Baker. Sarcolemmal and Mitochondrial K(ATP)Channels Mediate Cardioprotection in Chronically Hypoxic Hearts. Journal of Molecular and Cellular Cardiology (2001) 33, 1041-1045. Hypoxia from birth increases the resistance of the isolated neonatal heart to ischemia. We determined if increased resistance to ischemia was due to activation of sarcolemmal or mitochondrial K(ATP)channels. Rabbits (n=8/group) were raised from birth in a normoxic (F(I)O(2)=0.21) or hypoxic (F(I)O(2)=0.12) environment for 8-10 days and the heart perfused with Krebs-Henseleit bicarbonate buffer. A mitochondrial-selective K(ATP)channel blocker 5-hydroxydecanoate (5-HD) (300 micromol/l) or a sarcolemmal-selective K(ATP)channel blocker HMR 1098 (30 micromol/l) were added alone or in combination for 20 min prior to a global ischemic period of 30 min, followed by 35 min reperfusion. Recovery of ventricular developed pressure was higher in chronically hypoxic than normoxic hearts. 5-HD and HMR 1098 partially reduced the cardioprotective effect of chronic hypoxia, but had no effect in normoxic hearts. The combination of 5-HD and HMR 1098 abolished the cardioprotective effect of chronic hypoxia. We conclude that both sarcolemmal and mitochondrial K(ATP)channels contribute to cardioprotection in the chronically hypoxic heart.
Author List
Kong X, Tweddell JS, Gross GJ, 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
AnimalsAnti-Arrhythmia Agents
Benzamides
Decanoic Acids
Heart
Hemodynamics
Hydroxy Acids
Hypoxia
Ischemia
Mitochondria
Myocardium
Oxygen
Perfusion
Potassium
Potassium Channels
Rabbits
Sarcolemma
Time Factors
