scholarly journals Development of a Species-Specific Model of Cerebral Hemodynamics

2005 ◽  
Vol 6 (3) ◽  
pp. 181-195
Author(s):  
Silvia Daun ◽  
Thorsten Tjardes
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Cardiac Output ◽  
Head Injuries ◽  
Cerebral Arteries ◽  
Specific Model ◽  
Cerebral Hemodynamics ◽  
Heart Frequency ◽  
Regulation Mechanisms ◽  
Species Specific

In this paper, a mathematical model for the description of cerebral hemodynamics is developed. This model is able to simulate the regulation mechanisms working on the small cerebral arteries and arterioles, and thus to adapt dynamically the blood flow in brain. Special interest is laid on the release of catecholamines and their effect on heart frequency, cardiac output and blood pressure. Therefore, this model is able to describe situations of severe head injuries in a very realistic way.

scholarly journals Modelling, Analysis and Calculation of Cerebral Hemodynamics

2007 ◽  
Vol 8 (3) ◽  
pp. 205-223 ◽  
Author(s):  
Silvia Daun ◽  
Thorsten Tjardes
Keyword(s):  
Periodic Solutions ◽  
Cerebral Arteries ◽  
Cerebral Hemodynamics ◽  
Human Model ◽  
Hopf Bifurcations ◽  
Plateau Waves ◽  
Modelling Analysis ◽  
Regulation Mechanisms ◽  
Existence Of Periodic Solutions ◽  
Injury Models

Mathematical models of cerebral hemodynamics, applicable to humans and rats have been developed and analysed with the purpose of reaching a deeper insight to which degree experimental results on rats can be extrapolated to humans and to clinical management of patients. These models include regulation mechanisms involving the small cerebral arteries and arterioles, flow autoregulation, as well as CO2and NO reactivity. Bifurcation analysis was conducted on both models.The human model includes Hopf-bifurcations, which allow for the existence of periodic solutions with a time scale comparable to Lundberg's plateau waves in intracranial pressure (Pic). By contrast, the rat model does not manifest Hopf-bifurcations and thus does not predict the existence of periodic solutions with critical highPic.Therefore the model questions the relevance of rodent injury models to predict human physiology following TBI.

Effects of high-frequency prefrontal rTMS on heart frequency rates and blood pressure in schizophrenia

2021 ◽  
Author(s):  
Mattia Campana ◽  
Elias Wagner ◽  
Thomas Wobrock ◽  
Berthold Langguth ◽  
Michael Landgrebe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Frequency ◽  
Heart Frequency

scholarly journals The cardiac output from blood pressure algorithms trial*

2009 ◽  
Vol 37 (1) ◽  
pp. 72-80 ◽  
Author(s):  
James X. Sun ◽  
Andrew T. Reisner ◽  
Mohammed Saeed ◽  
Thomas Heldt ◽  
Roger G. Mark
Keyword(s):  
Blood Pressure ◽  
Cardiac Output

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

2005 ◽  
Vol 288 (6) ◽  
pp. R1637-R1648 ◽  
Author(s):  
Peter E. Hammer ◽  
J. Philip Saul
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Volume ◽  
Low Frequency ◽  
Pressure Waves ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Gain Margin ◽  
The Stability

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

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