While some studies opt to evaluate BRS in the supine position, its evaluation in the orthostatic position seems to be more appropriate, as
baroreceptor activation depends on BP oscillation.
3) The
baroreceptor response of high vascular tone that occurs with the bolus.
This increased adrenergic drive could be due to
baroreceptor dysfunction, increased sensitivity of vascular chemoreceptors, and decreased parasympathetic activity.
BNP can promote natriuresis, inhibit secretion of antidiuretic hormone and sympathetic nerve impulse, and regulate
baroreceptor. Most of the studies have suggested that the level of NT-pro BNP of patients with acute cerebral infarction was higher than that of normal people.
Early effects of oral salt on plasma volume, orthostatic tolerance, and
baroreceptor sensitivity in patients with syncope.
Elevated BP recorded after the injection of the high-dose venom increases the firing rate of the
baroreceptor nerves and results in a decreased output from the sympathetic regions and an increased output from the parasympathetic regions of the brain.
Propofol decreases blood pressure (2-6) by decreasing preload and afterload, (7,8), cardiac output and systemic vascular resistance (9,10) due to inhibition of sympathetic vasoconstriction (11) and impairment of
baroreceptor reflex regulatory system.
Although
baroreceptor reflex was affected by gender and age,[25] further studies investigating the relationship between
baroreceptor sensitivity and ICH outcome according to type or location are required.
The physiological mechanisms responsible for PEH were not analyzed in the present study; however, some studies (7,31) suggest that the hypotensive response is caused by
baroreceptor action, reduced total peripheral vascular resistance, and decreased cardiac output.
They postulated that a handstand is likely to cause vagal stimulation by transiently increasing thoracic pressure, stimulating
baroreceptor activity in the aortic arch and carotid bodies and resulting in increased parasympathetic tone.
Although underlying mechanisms for hyperperfusion remain undetermined, possible pathophysiology for CHPS has been suggested to be the impaired autoregulation, endothelial dysfunction mediated by free radicals, breakdown of the
baroreceptor reflex, and breakdown of bloodbrain-barrier (BBB), which results from a rapid increase in cerebral blood flow [15, 16].