Abstract
Oxygen deficiency in heart muscle is most commonly induced by reduction in coronary flow, referred to as ischemia. As contrasted to hypoxia or anoxia in which flow of blood with low or zero oxygen tension is maintained, ischemia leads to accumulation of metabolic products that further modify rates of biochemical reactions. After periods of severe ischemia ranging from 30 minutes to 1 hour or more, irreversible damage occurs. Damage of this severity is characterized by disruption of the plasma membrane that is preceded by swelling of both the cell and mitochondria. Concurrently, the myofibrils and intercellular junctions are disrupted, and there is margination of nuclear chromatin. Reperfusion of an irreversibly-injured cell leads to accumulation of Ca++ within the mitochondria and failure to recover contractile activity.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
R. B. Jennings, and C. E. Ganote, Mitochondrial structure and function in acute myocardial ischemic injury, Circ. Res. 38: Suppl 1:180–191 (1976).
C. deDuve, and H. Beaufay, Tissue fractionation studies, Influence of ischemia on the state of some bound enzymes in rat liver, Biochem. J. 73: 610–616 (1959).
E. G. Leighty, C.D. Stoner, M. M. Ressallat, G. T. Passananti, and H. D. Sirak, Effects of acute asphyxia and deep hypothermia on the state of binding of lysosomal acid hydrolases in canine cardiac muscle, Circ. Res. 21: 59–64 (1967).
M. A. Riccuitti, Lysosomes and myocardial cellular injury. Am J. Cardio. 30: 498–502 (1972).
S. Hoffstein, G. Weissman, and A. C. Fox, Lysosomes in myocardial infarction: Studies by means of cytochemistry and subcellular fractionation with observations on the effects of methylprednisolone, Circulation 53: Suppl 1:134–140 (1976).
L. P. McAllister, B. L. Munger, and J. R. Neely, Electron microscopic observations and acid phosphatase activity in the ischemic rat heart, J. Mol. Cell. Cardiol 9: 353–364 (1977).
B. Chua, R. L. Kao, D. E. Rannels, and H. E. Morgan, Inhibition of protein degradation by anoxia and ischemia in perfused rat hearts, J. Biol. Chem. 254: 6617–6623 (1979).
J. R. Neely, and H. E. Morgan, Relationship between carbohydrate and lipid metabolism and the energy balance of heart muscle. Ann. Rev. Physiol. 36: 413–459 (1974).
K. F. LaNoue, and A. C. Schoolwerth, Metabolite transport in mitochondria, Ann. Rev. Biochem. 48:871–922 (1979).
S. Mochizuki, and J. R. Neely, Control of glyceraldehyde-3-P dehydrogenase in cardiac muscle, J. Mol. Cell Cardiol. 11: 221–236 (1979).
M. J. Rovetto, W. F. Lamberton, and J. R. Neely, Mechanisms of glycolytic inhibition in ischemic rat hearts, Circ. Res. 37: 742–751 (1975).
J. R. Neely, J. T. Whitmer, and M. J, Rovetto, Effect of coronary blood flow on glycolytic flux and intracellular pH in isolated rat hearts, Circ. Res. 37: 733–741 (1975).
M. F. Oliver, V. A. Kurien, and T. W. Greenwood, Relation between serum-free fatty acids and arrhythmias and death after acute myocardial infarction, Lancet 1: 710–714 (1968).
J. A. Idell-Wenger, and J. R. Neely, Regulation of uptake and metabolism of fatty acids by muscle, in: “Disturbances in Lipid and Lipoprotein Metabolism,” J. M. Dietschy, A. M. Gotto Jr., and J. A. Ontko, eds., American Physiological Society, Bethesda, pp 269–284 (1978).
J. W. DeJong, and W. C. Hulsman, A comparative study of palmitoyl CoA synthetase activity in rat liver, heart and gut mitochondrial and microsomal preparation, Biochem Biophys Acta 197: 127–135 (1970).
J. W. DeJong, and W. C., Hulsman, Effects of Nagarse, adenosine and hexokinase on palmitate activation and oxidation, Biochem. Biophys. Acta 210: 499–501 (1970).
S. V. Pande, Reversal by CoA of palmityl-CoA inhibition of long chain acyl-CoA synthetase activity, Biochem Biophys. Acta 306: 15–20 (1973).
J. F. Oram, J. I. Wenger, and J. R. Neely, Regulation of long chain fatty acid activation in heart muscle, J. Biol. Chem. 250: 73–78 (1975).
H. H. Chong, and S. V. Pande, On the specificity of the inhibition of adenine nucleotide translocase by long chain acyl-coenzyme A esters, Biochem. Biophys. Acta 369:86–94 (1974).
B. Chua, and E. Shrago, Reversible inhibition of adenine nucleotide translocation by long chain acyl CoA esters in bovine heart mitochondria and inverted submitochondrial particles, J. Biol. Chem. 252:6711–6714 (1977).
F. Morel, G. Lauquin, J. Lunardi, J. Duszynski, and P. V. Vignais An appraisal of the functional significance of the inhibitory effect of long chain acyl-CoAs on mitochondrial transports, FEBS Lett.39:133–138 (1974).
J. M. J. Lamers, and W. C. Hulsmann, Inhibition of (Na+ + Ka+)- stimulated ATPase of heart by fatty acids, J. Mol. Cell. Card. 9: 343–346 (1977).
J. M. Wood, B. Bush, B. J. R. Pitts, and A. Schwartz, Inhibition of bovine heart Na+, K+ — ATPase by palmitylcarnitine and palmityl-CoA, Biochem. Biophys. Res. Commun. 74:677–684 (1977).
R. Kao, D. E. Rannels, and H. E. Morgan, Effects of anoxia and ischemia on protein synthesis in perfused rat hearts, Circ. Res. 38: Suppl 1: 124–130 (1976).
H. E. Morgan, D. E. Rannels, and E. E. McKee, Protein metabolism of the heart, in: “Handbook of Physiology — The Cardiovascular System,” R. M. Berne, ed., American Physiological Society, Bethesa, pp 845–871 (1979).
H. E. Morgan, B. Chua, and C. J. Beinlich, Regulation of protein degradation in heart, in: “Degradative Processes in Heart and Skeletal Muscle,” K. Wildenthal, ed., North Holland Biomedical Press, Amsterdam, pp 87–112 (1980).
K. Wildenthal, Lysosomes and lysosomal enzymes in the heart, in: “Lysosomes in Biology and Pathology,” J. T. Dingle and R. T. Deans, eds., Elsevier Publishing Company, Inc., New York, pp 167–190 (1975).
D. E. Rannels, R. Kao, and H. E. Morgan, Effect of insulin on protein turnover in heart muscle, J. Biol. Chem. 250: 1694–1701 (1975).
L. S. Jefferson, D. E. Rannels, B.LL. Munger, and H. E. Morgan, Insulin in the regulation of protein turnover in heart and skeletal muscle, Fed. Proc. 33: 1098–1104 (1974).
E. H. Williams, R. L. Kao, and H. E. Morgan, Protein degradation and synthesis during recovery from myocardial ischemia, Am. J. Physiol. (Endocrinol. Metab. 3) 240: E268–E273 (1981).
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1984 Springer Science+Business Media New York
About this chapter
Cite this chapter
Morgan, H.E. (1984). Biochemical Mechanisms of Altered Metabolism in Ischemic Heart. In: Chazov, E.I., Smirnov, V.N., Oganov, R.G. (eds) Cardiology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1824-9_3
Download citation
DOI: https://doi.org/10.1007/978-1-4757-1824-9_3
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-1826-3
Online ISBN: 978-1-4757-1824-9
eBook Packages: Springer Book Archive