Effect of ischemic preconditioning on mitochondrial oxidative phosphorylation and high energy phosphates in rat hearts. 1996

M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.

The ability of ischemic preconditioning (IP) to protect the myocardium against prolonged ischemia may derive from improved energy balance. We therefore examined myocardial energy metabolism and mitochondrial oxidative phosphorylation in isolated perfused rat hearts which were either subjected (IP group), or not subjected (control group), to preconditioning prior to 30 min sustained ischemia and 30 min reperfusion. Preconditioning was achieved with two cycles of 5 min ischemia followed by 5 min reperfusion. Recovery of myocardial function was significantly greater, and creatine kinase release was significantly lower, in the IP group. Although ATP hydrolysis during the sustained ischemia remained unchanged in both groups, greater preservation of high energy phosphate (eg. ATP and CP) was observed in the IP group after reperfusion. CP content immediately after preconditioning greatly exceeded pre-ischemic values. Lactate production during the sustained ischemia was significantly lower in the IP group, suggesting a decrease in anaerobic glycolysis and a probable attenuation of intracellular acidosis. Oligomycin-sensitive mitochondrial ATPase activity in the control group was significantly decreased both after the sustained ischemia and the reperfusion, but in the IP group it did not change after the preconditioning, sustained ischemia, or reperfusion. Although atractyloside-inhibitable adenine nucleotide translocase activity was markedly decreased during sustained ischemia in both groups, its activity was significantly higher after reperfusion in the IP group. These data suggest that (1) mitochondrial ATPase contributes only slightly to ATP depletion during sustained ischemia, (2) both the CP overshoot phenomenon and the decrease in anaerobic glycolysis can be attributable to cardioprotection during the sustained ischemia, and (3) the preservation of ATPase and adenine nucleotide translocase activities may be a possible explanation for the restoration of high energy phosphates after sustained ischemia-reperfusion injury in the preconditioned hearts of rats.

UI MeSH Term Description Entries
D007773 Lactates Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.
D008297 Male Males
D008929 Mitochondria, Heart The mitochondria of the myocardium. Heart Mitochondria,Myocardial Mitochondria,Mitochondrion, Heart,Heart Mitochondrion,Mitochondria, Myocardial
D010085 Oxidative Phosphorylation Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds. Phosphorylation, Oxidative,Oxidative Phosphorylations,Phosphorylations, Oxidative
D010725 Phosphocreatine An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996) Creatine Phosphate,Neoton,Phosphocreatine, Disodium Salt,Phosphorylcreatine,Disodium Salt Phosphocreatine,Phosphate, Creatine
D003401 Creatine An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as CREATININE in the urine.
D003402 Creatine Kinase A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins. Creatine Phosphokinase,ADP Phosphocreatine Phosphotransferase,ATP Creatine Phosphotransferase,Macro-Creatine Kinase,Creatine Phosphotransferase, ATP,Kinase, Creatine,Macro Creatine Kinase,Phosphocreatine Phosphotransferase, ADP,Phosphokinase, Creatine,Phosphotransferase, ADP Phosphocreatine,Phosphotransferase, ATP Creatine
D005069 Evaluation Studies as Topic Works about studies that determine the effectiveness or value of processes, personnel, and equipment, or the material on conducting such studies. Critique,Evaluation Indexes,Evaluation Methodology,Evaluation Report,Evaluation Research,Methodology, Evaluation,Pre-Post Tests,Qualitative Evaluation,Quantitative Evaluation,Theoretical Effectiveness,Use-Effectiveness,Critiques,Effectiveness, Theoretical,Evaluation Methodologies,Evaluation Reports,Evaluation, Qualitative,Evaluation, Quantitative,Evaluations, Qualitative,Evaluations, Quantitative,Indexes, Evaluation,Methodologies, Evaluation,Pre Post Tests,Pre-Post Test,Qualitative Evaluations,Quantitative Evaluations,Report, Evaluation,Reports, Evaluation,Research, Evaluation,Test, Pre-Post,Tests, Pre-Post,Use Effectiveness
D006019 Glycolysis A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH. Embden-Meyerhof Pathway,Embden-Meyerhof-Parnas Pathway,Embden Meyerhof Parnas Pathway,Embden Meyerhof Pathway,Embden-Meyerhof Pathways,Pathway, Embden-Meyerhof,Pathway, Embden-Meyerhof-Parnas,Pathways, Embden-Meyerhof
D000226 Mitochondrial ADP, ATP Translocases A class of nucleotide translocases found abundantly in mitochondria that function as integral components of the inner mitochondrial membrane. They facilitate the exchange of ADP and ATP between the cytosol and the mitochondria, thereby linking the subcellular compartments of ATP production to those of ATP utilization. ADP,ATP Carrier,ADP,ATP Translocator Protein,Adenine Nucleotide Translocase,ADP Translocase,ATP Translocase,ATP,ADP-Carrier,ATP-ADP Translocase,Adenine Nucleotide Carrier (Mitochondrial),Mitochondrial ADP-ATP Carriers,ADP-ATP Carriers, Mitochondrial,Mitochondrial ADP ATP Carriers

Related Publications

M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
September 1979, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.),
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
September 2001, American journal of physiology. Heart and circulatory physiology,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
May 2004, Canadian journal of physiology and pharmacology,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
January 2012, Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
October 2006, Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
July 1994, Circulation research,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
June 1980, Mayo Clinic proceedings,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
August 2013, American journal of physiology. Heart and circulatory physiology,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
June 1996, Japanese circulation journal,
M Kobara, and T Tatsumi, and S Matoba, and Y Yamahara, and C Nakagawa, and B Ohta, and T Matsumoto, and D Inoue, and J Asayama, and M Nakagawa
January 1990, Industrial health,
Copied contents to your clipboard!