Conclusion - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 803

of breathing. Whereas chemical control of breathing relies on arterial and brain
partial pressure in O 2 and CO 2 and pH sensed by peripheral and central chemore-
ceptors, the behavioral control of breathing is based on cues received from different
sites (e.g., cortical and subcortical regions and hypothalamus, as well as proprio-
and nociceptors). The behavioral control of breathing regulates breathing either by
direct control of respiratory motoneurons (corticospinal control of respiration) or by
modulation of respiratory centers in the brainstem via the reticular activating system
(or extrathalamic control modulatory system). In addition, the behavioral control
can modulate the chemical control to optimize breathing to the body's needs.
The heart is capable of beating independently of any nervous or hormonal influ-
ences, hence is endowed with intrinsic automaticity. Yet, its activity is influenced by
nervous signals as well as by regulatory chemicals. Like other muscle or nerve cells,
cardiomyocytes are excitable cells that synchronously contract at a given rate when
their plasma membrane depolarizes upon the arrival of electrochemical impulses —
action potentials — that are initiated in and run through the nodal tissue.
Like breathing, nervous control of the heart relies on parasympathetic fibers that
travel in vagus nerves and sympathetic nerves. The vagus nerve operates as a cardiac
inhibitor, whereas sympathetic nerves are cardiac exciters. The sympathetic nervous
system supply to the heart leaves the spinal cord at the first 4 thoracic (T1-T4)
vertebra.
The sympathetic nervous system causes bronchodilation and vasoconstriction,
thus diverting blood flow away from some vascular compartments to others, but it
promotes vasodilation for the coronary arteries, and increases the cardiac frequency
and myocardium contractility. On the other hand, the parasympathetic nervous
system provokes bronchoconstriction and vasodilation.
At the effector organs, sympathetic postganglionic neurons release noradrenaline
(or norepinephrine), along with other cotransmitters such as ATP, among others.
Noradrenaline binds to adrenergic receptors (Table 14.3 ). Acetylcholine is the
neurotransmitter for both preganglionic sympathetic and parasympathetic neurons
as well as for postganglionic parasympathetic neurons. Acetylcholine targets mus-
carinic receptors on the plasma membrane of effector cells (Table 14.4 ). At the
adrenal medulla, an endocrine gland, presynaptic neurons release acetylcholine
that binds to nicotinic receptors, i.e., ligand-gated ion channels. Stimulated adrenal
medulla releases adrenaline (epinephrine) into the blood stream. Adrenaline targets
also adrenergic receptors, thereby enhancing sympathetic activity.
Any modeling and simulation tests explore a biological event at a given
time. In the case of physiological flows, numerical simulations use computational
domains based on the three-dimensional reconstruction of organs of interest from a
medical imaging data set to get a patient-specific geometry, as organ configuration
varies strongly between human subjects. However, medical imaging, an element of
personnalized medicine, not only captures data at a given moment, but also yields a
model of real anatomy.
Therefore, a wide gap still exists between competences, on the one hand,
in modeling and numerical analysis, development of appropriate simulation al-
gorithms, softwares, and coupling platforms for solving multiscale, multiphysics
problems related to complex behavior and non-linear dynamics that incorporate