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Optimal Circulation - Cells Contribution to Arterial Pressure (Hardcover)
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Optimal Circulation - Cells Contribution to Arterial Pressure (Hardcover)
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Prevailing physiological concepts (PPC) of blood circulation
consider the cardiovascular system (CVS) an autonomous system that
has its own goal and mechanisms for achieving it. Physiologists
agreed that complex neural and humoral controllers of a mean
arterial pressure (MAP) indirectly alter the blood flows for
satisfying cellular needs. However, PPCs are incapable of
explaining the causes of long-term shifts of an MAPs rest level. In
particular, this affects current understanding and cure
technologies of arterial hypertension (AH). Considering AH as a
disease, physicians seek a cure that effectively decreases the
elevated pressure. This gave rise to the palliative cure softening
of AH symptoms without an understanding of AHs primary causes. But
this strategy, working until the patient intakes antihypertensive
drugs, often leads to AHs further development, and in extreme cases
current antihypertensive drugs are helpless. These limitations of
PPC are forced to seek a circulations extended physiological theory
(EPT), explaining the mechanisms of both normal and altered MAPs.
In the EPT presented in the book, CVS is considered a constituent
part of a more complex functional super-system (FSS) that appeared
in a multi-cellular animal organism during the co-evolution of
specialized cells. The general goal of the FSS is to provide
optimal physiochemical and energy states of the cell cytoplasm. To
achieve this goal under a stochastic total and local variations of
cells activity, FSS should control: i) The cardiac output; ii) the
regional and local blood flows; and iii) the chemical composition
of both arterial and venous blood. Under chronic energy shortage,
FSS should also provide an adequate increasing of ATP-synthesis in
mitochondria of stagnated cells. So, under the ineffectiveness of
current mitochondria, FSS must enrich the arterial blood by
chemicals providing the biogenesis of mitochondria. However,
neither the energy providers nor the providers of blood chemistry
are properly involved in PC of the blood circulation. The EPT for
the first time integrates the hemodynamic and metabolic aspects of
cell life at the organism scale. It is proved that the CVS activity
is inversely associated with the activity mechanisms controlling
the rates of both pulmonary ventilation and erythropoiesis. Under
significant and chronic energy deficiency, the cells activate
additional FSS mechanisms, materially supporting the biogenesis of
mitochondria. The activity of FSS mechanisms forming the chemical
composition of arterial and venous blood is in reciprocal
relationships with the function of CVS. So, the EPT associates the
function of CVS with energy and metabolic problems in cells. The
EPT concerns both traditional and additional determinants of the
MAP level. It is proved that stochastic combinations of these
determinants force the MAP level to float. In particular, both the
mitochondrial insufficiency and the chemical contamination of
cytoplasm are capable of causing AH. The normal arterial pressure
is always individual. Before correcting the altered arterial
pressure, a complex medical examination for ascertaining the
mitochondrial function, the status of the FSS mechanisms is
recommended. The diagnosis of AH should be reoriented for detecting
cellular abnormalities. The therapy of AH should be targeted at
finding strategies for the optimizing the entire FSS function.
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