Basic Research in Cardiology

, Volume 77, Issue 1, pp 82–92 | Cite as

Metabolic changes in modified smooth muscle cells of rabbit carotid arteries

  • H. Heinle
  • F. Stowasser
  • E. Betz
Original Contributions


In the common carotid artery of rabbits, intimal myocyte proliferations were induced by daily repeated local electrical stimulation of the vessel wall in combination with a cholesterol containing diet given for 4 weeks. Some biochemical parameters of the morphologically modified intimal smooth muscle cells were studied and compared with those of samples obtained from nonstimulated tunica media of the contralateral carotid artery. The results show that in relation to dry weight both alkali extractable protein and DNA content of the proliferates are increased to about 125%. In the proliferates, the in-vivo tissue concentrations of glucose and glycogen are only 50–70% of the normal values, whereas the concentration of lactate is increased to about 160%. In-vitro incubation experiments of excised tissue samples from the intimal proliferates and normal media indicate that under an optimal supply of substrates the glucose uptake and lactate production of the proliferates are increased to 140% and 150%, respectively. This result provides evidence for an increased capacity of glycolysis in the proliferates, which in vivo may lead to a decrease in glucose concentration and to an increased concentration of lactate. This investigation shows that modified smooth muscle cells proliferating in the arterial intima exhibit an activated metabolism as seen in other models of arteriosclerosis.

Key words

model of arteriosclerosis electrical stimulation vascular smooth muscle cell proliferation modified myocytes glucose metabolism 


In der Arteria carotis communis von Kaninchen wurden durch wiederholte, lokale elektrische Reizung intimale Myozytenproliferate hervorgerufen. Einige Stoffwechselparameter der morphologisch modifizierten Intimamyozyten wurden verglichen mit denen glatter Muskelzellen, die aus der Media unstimulierter Gefäßabschnitte stammten. Die Ergebnisse zeigen, daß der Gehalt an DNA und alkaliextrahierbarem Protein in den Proliferaten um etwa 25% erhöht ist. Ebenso ist der laktatspiegel erhöht (etwa um 60%), während die Konzentrationen von Glukose und Glykogen auf etwa 50–70% der Normalwerte absinken. In-vitro-Inkubationen von Gewebeproben aus intimalen Proliferaten und normaler Media zeigen, daß die Glukoseaufnahme und die Laktatproduktion um 40 bzw. 50% gesteigert sind. Diese Ergebnisse lassen den Schluß zu, daß die Zellen des Proliferates eine erhöhte Glykolysekapazität aufweisen, die unter In-vivo-Verhältnissen zu einer verminderten Glukose- und Glykogenkonzentration und zu einem erhöhten Laktatgehalt im Gewebe führt. Das heißt, daß in Übereinstimmung mit anderen Arteriosklerosemodellen sich die morphologisch modifizierten Intimamyozyten auch durch einen gesteigerten Stoffwechsel von den normalen Mediamyozyten unterscheiden.


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  1. 1.
    Knieriem, H. J.: Immunhistochemische Untersuchungen zur Bedeutung der glatten Muskelzellen für die Pathohistogenese der Arteriosklerose des Menschen. Beitr. path. Anat.141, 4–18 (1970).Google Scholar
  2. 2.
    Wissler, R. W.: The arterial medial cell, smooth muscle or multifunctional mesenchyme? Circulation36, 1–4 (1967).PubMedGoogle Scholar
  3. 3.
    Ross, R., J. A. Glomset: The pathogenesis of atherosclerosis. New Engl. J. Med.295, 369–377 and 420–425 (1976).PubMedGoogle Scholar
  4. 4.
    Thomas, W. A., R. Jones, R. F. Scott, E. Morrison, F. Goodale, H. Imdi: Production of early atherosclerotic lesion in rats characterized by proliferation of “modified smooth muscle cells”. Exp. Mol. Pathol. Suppl.1, 40–61 (1963).Google Scholar
  5. 5.
    Riede, U. N., J. Staubesand. An unifying concept for the role of matrix vesicles and lysosomes in the formal pathogenesis of diseases of connective tissue and blood vessels. Beitr. Pathol.160, 3–37 (1977).PubMedGoogle Scholar
  6. 6.
    Buddecke, E.: Biochemie der Arterienwand. Verh. Dtsch. Ges. Kreislaufforschg.40, 15–24 (1975).Google Scholar
  7. 7.
    Morrison, E. S., R. F. Scott, M. Kroms, J. Frick: Glucose degradation in normal and atherosclerotic aortic intima-media. Atherosclerosis16, 175–184 (1972).PubMedGoogle Scholar
  8. 8.
    Stange, E., J. Papenberg: Changes in chemical and metabolic properties of rabbit aorta by dietary cholesterol, and saturated and polyunsaturated fats. Atherosclerosis29, 467–476 (1978).CrossRefPubMedGoogle Scholar
  9. 9.
    Betz, E., W. Scholote: Responses of vessel walls to chronically applied electrical stimuli. Basic Res. Cardiol.74, 10–20 (1979).PubMedGoogle Scholar
  10. 10.
    Eitel, W., G. Schmid, W. Schlote, E. Betz: Early arteriosclerotic changes of the carotid artery wall induced by electrostimulation. Path. Res. Prac.170, 211–229 (1980).Google Scholar
  11. 11.
    Schlote, W., J. W. Boellaard, E. Betz: Experimental atherosclerosis: The animal model and its relation to the human disease. Folia Angiologica28, 76–79 (1980).Google Scholar
  12. 12.
    Staubesand, J., G. Pott, U. Gerlach: Lysosomes and lysosomal enzymes in the arteries of rats suffering from genetic and renal hypertension. Path. Res. Pract.163, 109–114 (1978).PubMedGoogle Scholar
  13. 13.
    Jurrus, E. H., H. S. Weiss: In vitro tissue oxygen tensions in the rat aortic arch. Atherosclerosis29, 223–232 (1977).Google Scholar
  14. 14.
    Fritz, K. E., A. S. Daoud, J. M. Augustyn, J. Jarmolych: Morphological and biochemical differences among grossly-defined types of swine aortic atherosclerotic lesions induced by a combination of injury and atherogenic diet. Exp. Mol. Pathol.32, 61–72 (1980).CrossRefPubMedGoogle Scholar
  15. 15.
    Betz, E., J. Roth, W. Schlote: Proliferation of smooth muscle cells in long-term local electrical stimulation of carotid arteries. Folia Angiologica28, 28–31 (1980).Google Scholar
  16. 16.
    Keppler, D., K. Decker: Glycogen. In: “Methoden der enzymatischen Analyse” (Bergmeyer, H. U., ed.), 3. Aufl., II. Bd., 1171–1176, Verlag Chemie (Weinheim 1974).Google Scholar
  17. 17.
    Bergmeyer, H. U., E. Bert, F. Schmidt, H. Stork: Glucose. In: “Methoden der enzymatischen Analyse” (Bergmeyer, H. U., ed.), 3. Aufl., II. Bd., 1241–1246, Verlag Chemie (Weinheim 1974).Google Scholar
  18. 18.
    Gutmann, I., A. W. Wahlefeld: Lactat. In “Methoden der enzymatischen Analyse” (Bergmeyer, H. U., ed.), 3. Aufl., II. Bd., 1510–1514, Verlag Chemie (Weinheim 1974).Google Scholar
  19. 19.
    Puzas, J., D. B. P. Goodmann: A rapid assay for cellular desoxyribonucleic acid. Anal. Biochem.86, 50–55 (1978).CrossRefPubMedGoogle Scholar
  20. 20.
    Lowry, O. H., N. J. Rosebrough, A. L. Farr, R. J. Randall: Protein measurement with the Folinphenolreagent. J. Biol. Chem.193, 265–275 (1951).PubMedGoogle Scholar
  21. 21.
    Czok, R., W. Lamprecht: Pyruvat. In “Methoden der enzymatischen Analyse” (Bergmeyer, H. U., ed.), 3. Aufl., II. Bd., 1491–1496, Verlag Chemie (Weinheim 1974).Google Scholar
  22. 22.
    Numano, F., A. Sagara, M. Takenobu, S. Jamasawa, T. Shimamoto: Microbiochemical analysis of the arterial wall. Atherosclerosis17, 333–343 (1973).PubMedGoogle Scholar
  23. 23.
    Adams, C. W. M.: Vascular histochemistry in relation to the chemical and structural pathology of cardiovascular disease. Lloyd Luke (London 1967).Google Scholar
  24. 24.
    Morrison, A. D., L. Berwick, L. Orci, A. I. Winegrad: Morphology and metabolism of an aortic intima-media preparation in which an intact endothelium is preserved, J. Clin. Invest.57, 650–660 (1976).PubMedGoogle Scholar
  25. 25.
    Whereat, A. F.: Atherosclerosis and metabolic disorder in the arterial wall. Exp. Mol. Pathol.7, 233–247 (1967).CrossRefPubMedGoogle Scholar
  26. 26.
    Scott, R. F., E. S. Morrison, M. Kroms: Effect of cold shock on respiration and glycolysis in swine arterial tissue. Amer. J. Physiol.219, 1363–1365 (1970).PubMedGoogle Scholar
  27. 27.
    Schmiebusch, H., J. Staubesand, F. Steel: Ultrastructural and morphometric investigations into the arterial wall of the genetically hypertensive rat. Artery8, 294–304 (1980).PubMedGoogle Scholar
  28. 28.
    Staubesand, J., U. N. Riede: Ultrastrukturelles Reaktionsmuster der Gefäßwand mit besonderer Berücksichtigung der Mediamyocyten. In: “Gefäßwand, Rezidivprophylaxe, Raynaud Syndrom” (Ehringer, H., E. Betz, A. Bollinger E. Deutsch, ed.) p. 1–12, Witzstrock (Baden-Baden, Köln, New York 1979).Google Scholar
  29. 29.
    Staubesand, J., M. Fischer: Collagen dysplasia and matrix vesicles. Researches with the electronmicroscope into the problem of so-called “weakness of the vessel wall”. Path. Res. Pract.165, 374–391 (1979).PubMedGoogle Scholar
  30. 30.
    Chamley-Campbell, J. H., G. R. Campbell, R. Ross: Phenotype-dependent response of cultured aortic smooth muscle cells to serum mitogens. J. cell Biol.89, 379–383 (1981).CrossRefPubMedGoogle Scholar

Copyright information

© Dr. Dietrich Steinkopff Verlag 1982

Authors and Affiliations

  • H. Heinle
    • 1
  • F. Stowasser
    • 1
  • E. Betz
    • 1
  1. 1.Physiologisches Institut (I) der Universität TübingenTübingen

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