HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Cardioprotection by ischemic preconditioning preserves mitochondrial function and functional coupling between adenine nucleotide translocase and creatine kinase.

Abstract
M. N. Laclau, S. Boudina, J. B. Thambo, L. Tariosse, G. Gouverneur, S. Bonoron-Adèle, V. A. Saks, K. D. Garlid and P. Dos Santos. Cardioprotection by Ischemic Preconditioning Preserves Mitochondrial Function and Functional Coupling Between Adenine Nucleotide Translocase and Creatine Kinase. Journal of Molecular and Cellular Cardiology (2001) 33, 947-956. This study investigates the effect of ischemic preconditioning on mitochondrial function, including functional coupling between the adenine nucleotide translocase and mitochondrial creatine kinase, which is among the first reactions to be altered in ischemia. Three groups of Langendorff-perfused rat hearts were studied: a control group, a group subjected to 30 min ischemia followed by 15 min reperfusion, and a group subjected to ischemic preconditioning prior to 30 min ischemia and 15 min reperfusion. Ischemic preconditioning significantly delayed the onset and amplitude of contracture during ischemia, decreased enzymatic release, and improved the recovery of heart contractile function after reperfusion. Mitochondrial function was assessed in permeabilized skinned fibers. The protective effect of preconditioning was associated with preservation of mitochondrial function, as evidenced by maintenance of the high K(1/2)for ADP in regulation of mitochondrial respiration and V(max)of respiration, the near absence of respiratory stimulation by exogenous cytochrome c, and preservation of functional coupling between mitochondrial creatine kinase and adenine nucleotide translocase. These data suggest that ischemic preconditioning preserves the structure-function of the intermembrane space, perhaps by opening the mitochondrial ATP-sensitive K(+)channel. The consequence is preservation of energy transfer processes from mitochondria to ATP-utilizing sites in the cytosol. Both of these factors may contribute to cardioprotection and better functional recovery of preconditioned hearts.
AuthorsM N Laclau, S Boudina, J B Thambo, L Tariosse, G Gouverneur, S Bonoron-Adèle, V A Saks, K D Garlid, P Dos Santos
JournalJournal of molecular and cellular cardiology (J Mol Cell Cardiol) Vol. 33 Issue 5 Pg. 947-56 (May 2001) ISSN: 0022-2828 [Print] England
PMID11343417 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
CopyrightCopyright 2001 Academic Press.
Chemical References
  • Adenosine Diphosphate
  • Mitochondrial ADP, ATP Translocases
  • Creatine Kinase
  • Creatine
  • Oxygen
Topics
  • Adenosine Diphosphate (metabolism)
  • Animals
  • Cell Membrane (metabolism)
  • Creatine (metabolism)
  • Creatine Kinase (metabolism)
  • Heart (physiology)
  • Hemodynamics
  • Ischemic Preconditioning, Myocardial
  • Kinetics
  • Male
  • Mitochondria (metabolism)
  • Mitochondrial ADP, ATP Translocases (metabolism)
  • Myocardium (metabolism)
  • Oxygen (metabolism)
  • Perfusion
  • Phosphorylation
  • Protein Binding
  • Rats
  • Rats, Sprague-Dawley
  • Respiration
  • Time Factors

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: