Guyton Model: stress_relaxation
Catherine
Lloyd
Auckland Bioengineering Institute, University of Auckland
Model Status
This CellML model has been validated. Due to the differences between procedural code (in this case C-code) and declarative languages
(CellML), some aspects of the original model were not able to be encapsulated by the CellML model (such as the damping of variables).
This may affect the transient behaviour of the model, however the steady-state behaviour would remain the same. The equations in this
file and the steady-state output from the model conform to the results from the MODSIM program.
Model Structure
Arthur Guyton (1919-2003) was an American physiologist who became famous for his 1950s experiments in which he studied the physiology of
cardiac output and its relationship with the peripheral circulation. The results of these experiments challenged the conventional wisdom
that it was the heart itself that controlled cardiac output. Instead Guyton demonstrated that it was the need of the body tissues for
oxygen which was the real regulator of cardiac output. The "Guyton Curves" describe the relationship between right atrial pressures and
cardiac output, and they form a foundation for understanding the physiology of circulation.
The Guyton model of fluid, electrolyte, and circulatory regulation is an extensive mathematical model of human circulatory physiology,
capable of simulating a variety of experimental conditions, and contains a number of linked subsystems relating to circulation and its
neuroendocrine control.
This is a CellML translation of the Guyton model of the regulation of the circulatory system. The complete model consists of separate
modules each of which characterise a separate physiological subsystems. The Circulation Dynamics is the primary system, to which other
modules/blocks are connected. The other modules characterise the dynamics of the kidney, electrolytes and cell water, thirst and drinking,
hormone regulation, autonomic regulation, cardiovascular system etc, and these feedback on the central circulation model. The CellML code
in these modules is based on the C code from the programme C-MODSIM created by Dr Jean-Pierre Montani.
This particular CellML model describes the effect of stress relaxation on basic venous volume (V0). This model calculates the effect over
a period of time caused by excess volume (or too little volume) in the venous tree to cause changes in the volume holding capacity of the
venous tree when it is fully filled with blood but at zero pressure. In this model, there are two separate parallel stress relaxations of
the veins. One of these has a short time constant (SRK) and the other has a long time constant (SRK2).
model diagram
A systems analysis diagram for the full Guyton model describing circulation regulation.
model diagram
A schematic diagram of the components and processes described in the current CellML model.
There are several publications referring to the Guyton model. One of these papers is cited below:
Circulation: Overall Regulation, A.C. Guyton, T.G. Coleman, and H.J. Granger, 1972,
Annual Review of Physiology
, 34, 13-44. PubMed ID: 4334846
Guyton
Stress Relaxation
Description of Guyton stress relaxation module
2008-00-00 00:00
keyword
physiology
organ systems
cardiovascular circulation
stress relaxation
Guyton
Effect of Stress Relaxation on Basic Venous Volume (V0)
This section calculates the effect over a period of time caused by excess volume
(or too little volume) in the venous tree to cause changes in the volume holding
capacity of the venous tree when it is fully filled with blood but at zero pressure.
In this model, there are two separate parallel stress relaxations of the veins.
One of these has a short time constant (SRK) and the other has a long time constant (SRK2).
Encapsulation grouping component containing all the components in the Stress Relaxation Model. The inputs and
outputs of the Stress Relaxation Model must be passed by this component.
SR1 and SR2:
Calculation of the ultimate degree of change in basic venous volume to
be caused by the short-term stress relaxation factor with input to the
system equal to the instantaneous excess venous volume (VVE); a multiplier
factor controls the degree of stress relaxation that will occur (SR).
SR3, SR4, and SR5:
This is a delay circuit having a short time constant (SRK). The output of
this circuit (VV7) approaches the ultimate degree of stress relaxation
caused by short-term stress relaxation as calculated from Block SR2.
NB - REMOVED THE DAMPING FROM THE INTEGRAL!!!
SR1 and SR2:
Calculation of the ultimate degree of change in basic venous volume to
be caused by the short-term stress relaxation factor with input to the
system equal to the instantaneous excess venous volume (VVE); a multiplier
factor controls the degree of stress relaxation that will occur (SR).
SR3, SR4, and SR5:
This is a delay circuit having a short time constant (SRK). The output of
this circuit (VV7) approaches the ultimate degree of stress relaxation
caused by short-term stress relaxation as calculated from Block SR2.
NB - REMOVED THE DAMPING FROM THE INTEGRAL!!!
SR1A, SR2A, SR3A, AR4A, and SR5A:
Similar calculations to the above but this time with a long time constant
for stress relaxation (SRK2), and also having a separate variable for control
of the ultimate degree of the stress relaxation (SR2). The output of this
long time constant stress relaxation (VV6) along with the output from the
short time constant stress relaxation (VV7) are subtracted from the actual
venous volume (VVS) in Block CD15 in the hemodynamic section of the model.
SR1A, SR2A, SR3A, AR4A, and SR5A:
Similar calculations to the above but this time with a long time constant
for stress relaxation (SRK2), and also having a separate variable for control
of the ultimate degree of the stress relaxation (SR2). The output of this
long time constant stress relaxation (VV6) along with the output from the
short time constant stress relaxation (VV7) are subtracted from the actual
venous volume (VVS) in Block CD15 in the hemodynamic section of the model.