A Model of Electromechanical Coupling in the Small Intestine - Multiscale Computer Modeling in Biomechanics and Biomedical Engineering - page 200

The geometric model was limited to contain mostly linear basis functions in
order to minimize the degrees of freedom and therefore computation time. How-
ever, it would be of interest to evaluate how geometry and mechanical deformation
are affected by the order of the interpolation functions in the simulation, e.g., using
tri-cubic Hermite basis functions. Computing time may be reduced in the future by
using distributed memory multiprocessing for solving the finite deformation
problem. For example, the time consuming computation of the element stiffness
matrices can potentially be sped up by utilizing parallel computation techniques.
The electrical activity of intestinal motility is not limited to slow wave only. For
example, the changes in intestinal contractility also appear to be co-regulated by
other electrophysiological mediating mechanisms, such as spike activity is volt-
age-dependent and rapid oscillations during the plateau phase of the intestinal slow
waves, which apparently play an important role in mediating contractility during
certain stages of intestinal transit, e.g., during fasting [ 15 ]. However, as there is a
strong temporal relationship between slow waves, spikes, and contractions,
mechanical activation by slow waves could justifiably be treated in the temporal
domain as spike activation in this initial simulation. Nevertheless, it is still
important to include an intermediate spiking mechanism to realistically simulate
the autonomous control of a wider range of motility patterns in the small intestine.
In a recent study [ 34 ], spike patches were shown to propagate faster in the opposite
direction than the slow wave propagation, and spontaneously terminate spikes at
variable distances. At present, however, the cellular mechanisms behind spike
activity are poorly understood, and there are no existing models that simulate
intestinal spike activity. It would be interesting to incorporate these different
characteristics in future modeling studies to investigate how they affect intestinal
motility.
Even though voltage-dependent entry of Ca 2 þ has been postulated as one of the
main mechanisms of electromechanical coupling in the small intestine [ 44 , 49 ], the
enteric nervous system is also understood as another important regulator of gas-
trointestinal motility [ 31 ]. Incorporation of these neurological pathways will be an
important future direction towards an integrated mechanical model. Recently, an
extension to the bidomain model has been proposed as a possible framework to
bridge the present electromechanical modeling framework and future neural
models [ 10 ]. Much details of the neurologically mediated regulators of gastroin-
testinal motility still remain under investigations, and future modeling work will
be required to study these mechanisms as further details become clear.
The passive and active mechanical models implemented in this simulation
framework were developed by Bellini et al. [ 6 ] and adapted from Hunter
et al. [ 32 ]. [Ca 2 þ ] i acts as the intermediary between the electrical component and
the active mechanical component. Active tension is combined with the passive
tension to obtain the total tension at each gauss point. This is incorporated into the
finite deformation formulation to determine the resultant deformed geometry.
However, recent modeling studies have proposed more biophysically based

[Ca 2 þ ] i descriptions of the relationship between and cellular biomechanical