The High Pressure System of the Mammalian Circulation as a Dynamic Self-Organizing System

  • H. Schmid-Schönbein
  • S. Ziege
Part of the Springer Series in Synergetics book series (SSSYN, volume 55)


Highly stable fluctuations of arterial pressure are seen when rhythmic changes of heart rate and arterial blood pressure (measured indirectly by the non-invasive technique of photoplethysmography in the earlobe made hyperemic) are continuously measured during progressive relaxation of healthy subjects. Associated with physical and mental relaxation, the aperiodic rhythmic fluctuations of arterial pressure become entrained into a characteristic mode (frequency ca. 0.15Hz) in 27 out of 28 subjects lying comfortably. This rhythm could be clearly distinguished from respiratory sinus arrhythmia and respiratory blood pressure waves (ca. 0.25Hz) as well as from slower waves reflecting sympathetic activity (below 0.1Hz). This rhythm, further stabilized during early sleep, was regularly abolished by physical activity, standing, and exposure to various stimuli. The rhythm, also known to occur in postganglionic sympathetic muscle nerve activity, is discussed as a macroscopic projection of a synergetic process taking place in a cooperative mechanical system (the Windkessel vessels) exchanging information via afferent, central and efferent neuronal systems within the CNS. In generalizing the principle of the coherence of mesoscopic subsystems, we postulate that many systems (heart, arteries and various types of arterioles, afferent neurons, variable neuronal circuitry, interneurons and efferent neurons) get into progressive coherence due to mutual enslaving producing synergetic cooperativity. The energetic and informational aspects of progressive coherence during the reduction of central and cardiovascular drive (as control parameters) and of progressively active enslaving mechanisms (information compression) are discussed. A phenomenological model for a large synergetic system (“WKS-CNS ensemble”) is presented as the site of generation of stable synergetic order under the conditions of decreasing physical and mental activity.


Entropy Generation Respiratory Sinus Arrhythmia Postsynaptic Membrane Physical Rest Export Rate 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    K. Dittmers: Diplomarbeit, Fachhochschule Hamburg, 1988.Google Scholar
  2. 2.
    G. Sundlöf, B.G. Wallin: J. Physiol. 274., 621–637 (1978)Google Scholar
  3. 3.
    In animal experiments with non-anaesthetized sheep (not shown) a similar arterial blood pressure rhythm can be seen when the animals are at rest and is abolished completely by the procedure of extracellular CO2-removal, which renders the animals apnoic.Google Scholar
  4. 4.
    H. Haken: Information and Self-Organization. A Macroscopic Approach to Complex Systems (Springer, Berlin, Heidelberg, New York, London, Paris, Tokyo 1988)Google Scholar
  5. 5.
    H. Schmid-Schönbein: In: W. Bleifeld et al., Eds. Unstable Angina (Springer, Berlin, Heidelberg 1990), pp. 16–51CrossRefGoogle Scholar
  6. 6.
    W. Jänig: Ann. Rev. Physiol. 50, 525–539 (1988)CrossRefGoogle Scholar
  7. 7.
    W.R. Hess: Acta, Suppl. IV (1947)Google Scholar
  8. 8.
    E. Basar, Ch. Weiss: Vasculature and Circulation. The Role of Myogenic Reactivity in the Regulation of Blood Flow (Elsevier, North-Holland Biomedical Press Amsterdam, New York, Oxford 1981)Google Scholar
  9. For a future synergetic description of the cardiovascular system and its subsystems, many more cellular, nervous, metabolic and energetic details must be filled in. For reasons of spatial constraint, the synergistic role of only a few more dynamic links can be mentioned. While capillaries can be taken as a purely passive system, the venous return is probably a pivotal dynamic link. Its behavior limits — via the diastolic filling of the right and left atrium and ventricle — the continuous re-import of energy and matter into the WKVs. We reduce the contribution of the low pressure system (and that of the control systems for it) to a principle of energy conservation: it is assumed that the kinetic energy of the systemic and pulmonary venous blood is converted into the mechanical work required to do frictional work in extending the relaxed contractile apparatus of the right and left ventricle (a topic beyond the scope of the present treatise).Google Scholar
  10. 10.
    H. Schmid-Schonbein: In: J.L. Vincent, Ed. Update in Intensive Care and Emergency Medicine (Springer, Berlin, Heidelberg, New York, London, Paris, Tokyo, Hong Kong 1990), pp. 3–21Google Scholar
  11. 11.
    G. Burnstock: Acta Physiol. Scand. 126, 67–91 (1986)CrossRefGoogle Scholar
  12. The quantal release of neurotransmitters is taken as a “transport” of phemical signal down a preformed chemical gradient. The postsynaptic sequelae of transmitter action are assumed to modulate the import of energy (and informational order) from one “exited” into any subsequent neuron linked by a synaptic “funnel of information” to the former by an exchange of free energy. This follows from the fact that in any presynaptic apparatus, electrical energy pulses arriving in the form of action potentials are converted to chemical energy and back to electrical energy. Transmitter quanta are considered to result from chemical work done in the resting periods and as a reservoir of free energy (which is more appropriately called “convertible” or “convectible” energy).Google Scholar
  13. The extremely complex architecture of the reticular formation, in addition to the complexity of transmitter actions opens up the possibility that in the autonomous nervous system, due to the variable activation of excitatory and inhibitory neurons, information channels are far less “solidified” than in the somatic nervous system and that their ever changing plasticity in fact reflects their operation as a specific kind of “dissipative structure” (see contribution KOEPCHEN).Google Scholar
  14. 14.
    A.D. Loewy, K.M. Spyer: Central Regulation of Autonomic Functions (Oxford University Press 1990)Google Scholar
  15. 15.
    G.L. Gebber: In: K.M. Spyer Central Regulation of Autonomic Functions (Oxford University Press 1990), pp. 126–146Google Scholar
  16. 16.
    P.G. Gyyenet: In: K.M. Spyer Central Regulation of Autonomic Functions (Oxford University Press 1990), pp. 147–167Google Scholar
  17. 17.
    J.B. Cabot: In: K.M. Spyer Central Regulation of Autonomic Functions (Oxford University Press 1990), pp. 52–87Google Scholar
  18. 18.
    A.D. Loewy: In: A.D. Loewy, K.M. Spyer, Eds. Central Regulation of Autonomic Functions (Oxford University Press 1990), pp. 67–89Google Scholar
  19. 19.
    S.W. Mifflin: J. Physiol. 399, 349–367 (1988)Google Scholar
  20. 20.
    B.G. Wallin, D.L. Eckberg: Am. J. Physiol. 242, H185-H190 (1982)Google Scholar
  21. 21.
    E. Bath, L.E. Lindblad, B.G. Wallin: J. Physiol. 311, 551–564 (1981)Google Scholar
  22. 22.
    J. Fagius, B.G. Wallin, G. Sundlöf, C. Nerhed, S. Englesson: Brain 108, 423–438 (1985)CrossRefGoogle Scholar
  23. 23.
    Pool, R.: Science 243, 604–608 (1989)ADSCrossRefGoogle Scholar
  24. E. Basar, Ed.: In: Chaos in Brain Function (Springer Berlin, Heidelberg, New York, London, Paris, Tokyo, Hong Kong 1990), pp. 1–30Google Scholar
  25. 25.
    M. Pagani, F. Lombardi, S. Guzzetti, O. Rimoldi, R. Furlan, P. Pizzinelli, G. Sandrone, G. Malfatto, S. Dell’Orto, E. Piccaluga, M. Turiel, G. Baselli, S. Cerutti, A. Malliani: Circ. Res. 59, 178–193 (1986)Google Scholar
  26. 26.
    W. Cowley, J.F. Liard, A.C. Guyton: Circ. Res. 32, 564–565 (1973)Google Scholar
  27. 27.
    C.J. Mathias, H.L. Frankel: Ann. Rev. Physiol. 50, 577–92 (1988)CrossRefGoogle Scholar
  28. St. Ziege: MD Dissertationsschrift Rheinisch-Westfälische Technische Hochschule Aachen 1991Google Scholar
  29. H. Schmid-Schönbein, W. Rütten, H. Heidtmann (manuscript in preparation)Google Scholar
  30. 30.
    D.W. Richter, K.M. Spyer: In: A.D. Loewy, K.M. Spyer Central Regulation of Autonomie Functions (Oxford University Press 1990), pp. 189–207Google Scholar
  31. 31.
    G. Mancia, A.L. Mark: In: J.T. Shepherd, F.M. Abboud, Eds. Handbook of Physiology, Sect. 2 The Cardiovascular System (American Physiological Society, Bethesda, Maryland 1983)Google Scholar
  32. 32.
    H.S. Smyth, P. Sleight, G.W. Pickering: Circ. Res. 24r 109–121 (1969)Google Scholar
  33. We see a striking analogy with the synergetics of motor systems as studied by KELSO [34]. In order to go into functional coherence of bilateral spinal motor neuron pools, KELSO comes from below and has to increase the supraspinal “drive”. We reach the synergetic “window” of the slowly firing thoraco-lumbar preganglionic neurons by allowing the supraspinal drive to reduce itself (which occurs best once information compression intQ the inhibitory afffeirents sets in)Google Scholar
  34. 34.
    J.A.S. Kelso: Bull. Psychon. Soc. 18, 63 (1981)Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1991

Authors and Affiliations

  • H. Schmid-Schönbein
    • 1
  • S. Ziege
    • 1
  1. 1.Klinikum der RWTH AachenInstitut für PhysiologieAachenGermany

Personalised recommendations