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Modeling of Mechanisms Providing the Overall Control of Human Circulation
DOI:
https://doi.org/10.30564/ahpr.v4i1.4763Abstract
Multiple humoral and nervous mechanisms, each influencing the cardiovascular system (CVS) with its specific dynamics and power, had been evolutionarily saved both in animals and in human organisms. Most of such mechanisms are considered to be controllers of CVS’s function, but there is no concept clearly explaining the interaction of global and local controllers in intact human organisms under physiological or pathological conditions. Methodological and ethical constraints create practically insuperable obstacles while experiments on animals mainly concern artificial situations with certain switched-of mechanisms. Currently, mathematical modeling and computer simulations provide the most promising way for expanding and deepening our understanding of regulators’ interactions. As most of CVS’s models describe only partial control mechanisms, a special model (SM) capable of simulating every combination of control mechanisms is encouraged. This paper has three goals: i) to argue the uncial modeling concept and its physiological basis, ii) to describe SM, and iii) to give basic information about SM’s test research. SM describes human hemodynamics, which is under influence of arterial baroreceptor reflexes, peripheral chemoreceptor reflexes, central (CRAS) and local (lRAS) renin-angiotensin systems, local ischemia, and autoregulation of total brain flow. SM, performed in form of special software (SS), is tested under specific endogenous and/or exogenous alterations. The physiologist using SS can easily construct the desirable configuration of regulator mechanisms, their actual state, and scenarios of computer experiments. Tests illustrated the adequateness of SM, are the first step of SM’s research. Nuances of the interaction of modeled regulator mechanisms have to be illustrated in special publications.
Keywords:
Arterial pressure; Angiotensin Baroreflex; Chemoreflex; Hypertension; Renin-angiotensin systems; Ischemia; SimulationReferences
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