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

Content Provider	Semantic Scholar
Author	Laclau, Muriel N. Boudina, Sihem Thambo, Jean -Benoit Tariosse, Liliane Gouverneur, Gérard Bonoron-Adèle, Simone Saks, V. Garlid, Keith D. Santos, Pierre Dos
Copyright Year	2001
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.
Starting Page	526
Ending Page	530
Page Count	5
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://web.pdx.edu/~garlid/pdf/2001JMCC.pdf
PubMed reference number	11343417v1
Volume Number	33
Issue Number	5
Journal	Journal of molecular and cellular cardiology
Language	English
Access Restriction	Open
Subject Keyword	ADP/ATP translocase activity Adenine Nucleotide Translocase Adenine Nucleotides Adenosine Diphosphate Adenosine Triphosphate Biologic Preservation Contracture Control Groups Creatine Kinase Creatine Kinase, Mitochondrial Form Cytoplasmic matrix Energy Transfer Heart Hypoxic-Ischemic Encephalopathy Intermembranous space of mitochondrion Ischemia Mitochondria Mitochondrial Inheritance Muscle Contraction Nucleotide Transport Proteins Reperfusion Therapy Skin Tissue fiber Transient Ischemic Attack
Content Type	Text
Resource Type	Article