On the integration of the baroreflex control mechanism in a heterogeneous model of the cardiovascular system

2011 ◽  
Vol 28 (4) ◽  
pp. 412-433 ◽  
Author(s):  
P.J. Blanco ◽  
P.R. Trenhago ◽  
L.G. Fernandes ◽  
R.A. Feijóo
2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Luciano Gonçalves Fernandes ◽  
Paulo Roberto Trenhago ◽  
Pablo Javier Blanco ◽  
Raúl A Feijóo

1998 ◽  
Vol 274 (5) ◽  
pp. H1590-H1597 ◽  
Author(s):  
Giora Landesberg ◽  
Dan Adam ◽  
Yacov Berlatzky ◽  
Solange Akselrod

Step baroreceptor stimulation can provide an insight into the baroreflex control mechanism, yet this has never been done in humans. During carotid surgery under regional anesthesia, a step increase in baroreceptor stimulation occurs at carotid declamping immediately after removal of the intra-arterial atheromatous plaque. In 10 patients, the R-R interval and systolic and diastolic blood pressures (BP) were continuously recorded, and signals obtained within the time window from 10 min before until 10 min after carotid declamping were analyzed. Mean ± SD time signals, power spectra, and transfer and coherence functions before and after declamping were calculated. Immediately after carotid declamping, both heart rate (HR) and BP declined in an exponential-like manner lasting 10.3 ± 5.9 min, and their power spectra increased in the entire frequency range. Transfer function magnitude and coherence functions between BP and HR increased predominantly in the midfrequency region (∼0.1 Hz), with no change in phase function. Thus, in carotid endarterectomy patients, step increase in baroreceptor gain elicits a prolonged decline in HR and BP. Frequency analyses support the notion that the baroreflex control mechanism generates the midfrequency HR and BP variability, although other frequency regions are also affected.


1997 ◽  
Vol 273 (2) ◽  
pp. R457-R471 ◽  
Author(s):  
J. L. Segar

The autonomic nervous system is intimately involved in regulating cardiovascular function. Sensing mechanisms dispersed throughout the circulation, including arterial baroreceptors, low pressure receptors, and chemosensitive receptors, continually evoke reflexes designed to maintain cardiovascular homeostasis. Although there is a growing body of knowledge regarding neural regulation of the adult cardiovascular system, characterization and understanding of these physiological systems during development is limited. This review highlights developmental changes in the arterial and cardiopulmonary baroreflex during fetal and postnatal life and contrasts the function of these responses with those seen in the adult. Baroreceptors are functional in the immature animal and reset toward higher pressure levels with maturation. In our ovine model, the sensitivity of the efferent limb of the baroreflex is greatest during fetal life and decreases with postnatal development. As in the adult, angiotensin II and arginine vasopressin interact with the sympathetic nervous system early during development to alter baroreflex control of the cardiovascular system. However, the extent to which these hormonal systems influence autonomic reflexes during the fetal and newborn period appears vastly different than in the adult. Endogenous angiotensin II significantly contributes to resetting of the arterial baroreflex early in life, whereas even high circulating levels of vasopressin have little effect on baroreflex function until adulthood. Finally, the ability of cardiopulmonary mechanoreceptors to regulate cardiovascular function is impaired early in development, in sharp contrast to the heightened sensitivity of the arterial baroreflex at this stage of maturation. The potential importance of these autonomic reflexes on cardiovascular function during the perinatal period is highlighted.


2021 ◽  
Author(s):  
Timothy Hunter ◽  
Jermiah Joseph ◽  
Sanjay R Kharche ◽  
Daniel Goldman

Atrial fibrillation is a prevalent cardiac arrhythmia, and may reduce cerebral blood perfusion augmenting the risk of dementia. It is thought that cer- ebral arterial geometry variants play an important role in cerebral perfusion. This computational work investigated the role of geometric variants on cerebral blood flow in the presence of cardiac atrial fibrillation.A model consisting of a detailed cerebral and whole-body circulation, along with baroreflex control mechanism was developed. Cerebral perfusion based on vasculature geometry variations, represented by Circle of Willis variants, was simulated in the presence of atrial fibrillation conditions. Perfusion and its heter- ogeneity were quantified using segment-wise hypoperfusion events and mean perfusion at terminals.It was found that cerebral perfusion and the rate of hypoperfusion events strongly depends geometry variation as well as atrial fibrillation induced stochas- tic heart rates. The hypoperfusion events were specific to particular arteries in each variant. Our results, based on biophysical principles, suggest that cerebral vascular geometries modulate the impact of atrial fibrillation in cerebral perfu- sion. Further, our findings suggest potential clinical assessment sites.


2006 ◽  
Vol 940 (1) ◽  
pp. 338-347 ◽  
Author(s):  
EDUARDO MOACYR KRIEGER ◽  
GUSTAVO JOSÉ JUSTO SILVA ◽  
CARLOS EDUARDO NEGRÃO

1984 ◽  
Vol 66 (2) ◽  
pp. 233-235 ◽  
Author(s):  
M. A. Young ◽  
R. D. S. Watson ◽  
W. A. Littler

1. Intra-arterial pressure, baroreflex sensitivity and the baroreflex set point were measured in eight patients with essential hypertension during a control period and then after acute treatment (2 h after a 30 mg oral dose) and after chronic treatment (at least 2 months) with nicardipine hydrochloride, a calcium channel antagonist. 2. Mean intra-arterial blood pressure fell after the acute treatment from 130 ± 14 (sd) control to 118 ± 11 mmHg, P<0.05, and after chronic treatment to 112 ± 19 mmHg, P<0.05. Heart rate increased from 72 ± 11 control to 81 ± 16 beats/min, P<0.05, during acute treatment indicating activation of the baroreflex control mechanism, but returned to control values with chronic treatment (72 ± 11 control vs 69 ± 9 beats/min chronic), indicating a significant shift to the left of the baroreflex set point. There was no change in baroreflex sensitivity after either acute or chronic treatment (control 4.7, acute 4.3, chronic 5.1 ms/mmHg, P not significant for all values). 3. Nicardipine significantly reduces mean intraarterial pressure both acutely and chronically; the latter is associated with a return of the heart rate to control values due to resetting of the baroreflex control mechanism.


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