Limits...
A Model of Blood Pressure, Heart Rate, and Vaso-Vagal Responses Produced by Vestibulo-Sympathetic Activation.

Raphan T, Cohen B, Xiang Y, Yakushin SB - Front Neurosci (2016)

Bottom Line: Stochastic changes in threshold maintained the compensatory Baroreflex Sensitivity.Sudden decreases in Desired BP elicited non-compensatory VVRs with smaller pulse pressures, consistent with experimental data.It also shows that a VVR is generated when the vestibular input triggers a marked reduction in Desired BP.

View Article: PubMed Central - PubMed

Affiliation: Department of Computer and Information Science, Institute for Neural and Intelligent Systems, Brooklyn College, City University of New York New York, NY, USA.

ABSTRACT
Blood Pressure (BP), comprised of recurrent systoles and diastoles, is controlled by central mechanisms to maintain blood flow. Periodic behavior of BP was modeled to study how peak amplitudes and frequencies of the systoles are modulated by vestibular activation. The model was implemented as a relaxation oscillator, driven by a central signal related to Desired BP. Relaxation oscillations were maintained by a second order system comprising two integrators and a threshold element in the feedback loop. The output signal related to BP was generated as a nonlinear function of the derivative of the first state variable, which is a summation of an input related to Desired BP, feedback from the states, and an input from the vestibular system into one of the feedback loops. This nonlinear function was structured to best simulate the shapes of systoles and diastoles, the relationship between BP and Heart Rate (HR) as well as the amplitude modulations of BP and Pulse Pressure. Increases in threshold in one of the feedback loops produced lower frequencies of HR, but generated large pulse pressures to maintain orthostasis, without generating a VasoVagal Response (VVR). Pulse pressures were considerably smaller in the anesthetized rats than during the simulations, but simulated pulse pressures were lowered by including saturation in the feedback loop. Stochastic changes in threshold maintained the compensatory Baroreflex Sensitivity. Sudden decreases in Desired BP elicited non-compensatory VVRs with smaller pulse pressures, consistent with experimental data. The model suggests that the Vestibular Sympathetic Reflex (VSR) modulates BP and HR of an oscillating system by manipulating parameters of the baroreflex feedback and the signals that maintain the oscillations. It also shows that a VVR is generated when the vestibular input triggers a marked reduction in Desired BP.

No MeSH data available.


Related in: MedlinePlus

(A) Resting Blood Pressure response (BP) over 1 s time scale showing the triangular shapes of diastolic to systolic transitions. (B,C) BP variations over 10 s (B) and 40 s (C) scale. Vasovagal Response in BP (D) and HR (E) in response to ± 3 mA 0.025 Hz sinusoidal Galvanic Vestibular Stimulation (sGVS). This stimulus (F) generated a VVR, which is characterized by a transient decline in BP (D) followed by a decline in HR (E). The two vertical lines represent the start and stop of stimulation, respectively. The low level of HR outlasted the low level of BP (D,E). There was also a transient drop in BP (G) and HR (H) in response to nose up tilt of 60° (I). The tilt up and back are shown by the two vertical lines, respectively. The transient drops in BP are generally slower than during sGVS, but the recovery follows a similar time course where HR rises to baseline values slower than BP (G,H).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4814511&req=5

Figure 1: (A) Resting Blood Pressure response (BP) over 1 s time scale showing the triangular shapes of diastolic to systolic transitions. (B,C) BP variations over 10 s (B) and 40 s (C) scale. Vasovagal Response in BP (D) and HR (E) in response to ± 3 mA 0.025 Hz sinusoidal Galvanic Vestibular Stimulation (sGVS). This stimulus (F) generated a VVR, which is characterized by a transient decline in BP (D) followed by a decline in HR (E). The two vertical lines represent the start and stop of stimulation, respectively. The low level of HR outlasted the low level of BP (D,E). There was also a transient drop in BP (G) and HR (H) in response to nose up tilt of 60° (I). The tilt up and back are shown by the two vertical lines, respectively. The transient drops in BP are generally slower than during sGVS, but the recovery follows a similar time course where HR rises to baseline values slower than BP (G,H).

Mentions: The model was derived from data showing that BP is a temporally repetitive waveform that can be analyzed at different time scales. At the smallest time scale (1 s) there are systolic to diastolic transitions whose waveform is approximately triangular in shape and can be reproduced by the relaxation oscillator developed in this study (Figure 1A). The idea that the heart oscillation can be described by a relaxation oscillator was first introduced by Van der Pol and Van der Mark (1928) and models based on this idea are discussed by Noble and Noble (2011). An important point of the model presented here is that the shape of the systolic/diastolic waveform is not determined strictly by the heart. It is determined by an internal model (relaxation oscillator) through a feedback neural network, which mimics the oscillation features of the heart. The feedback mechanisms implement closed loop control and then activate actuators through nonlinear mechanisms that control the constriction of the vascular beds, which has been referred to as peripheral vascular resistance. The feedback from the baroreceptors is compared with the output of the internal model to implement model-reference control. At a larger time scale (10 s), oscillations in systolic amplitude related to breathing can be observed (Figure 1B). There are also small amplitude very low frequency oscillations in the systolic and diastolic BP that have been termed Mayer waves (Mayer, 1876; Myers et al., 2001; Julien, 2006) as well as low frequency oscillations, which are associated with VVR's, which we have termed VasVagal Oscillations (Yakushin et al., 2014).


A Model of Blood Pressure, Heart Rate, and Vaso-Vagal Responses Produced by Vestibulo-Sympathetic Activation.

Raphan T, Cohen B, Xiang Y, Yakushin SB - Front Neurosci (2016)

(A) Resting Blood Pressure response (BP) over 1 s time scale showing the triangular shapes of diastolic to systolic transitions. (B,C) BP variations over 10 s (B) and 40 s (C) scale. Vasovagal Response in BP (D) and HR (E) in response to ± 3 mA 0.025 Hz sinusoidal Galvanic Vestibular Stimulation (sGVS). This stimulus (F) generated a VVR, which is characterized by a transient decline in BP (D) followed by a decline in HR (E). The two vertical lines represent the start and stop of stimulation, respectively. The low level of HR outlasted the low level of BP (D,E). There was also a transient drop in BP (G) and HR (H) in response to nose up tilt of 60° (I). The tilt up and back are shown by the two vertical lines, respectively. The transient drops in BP are generally slower than during sGVS, but the recovery follows a similar time course where HR rises to baseline values slower than BP (G,H).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4814511&req=5

Figure 1: (A) Resting Blood Pressure response (BP) over 1 s time scale showing the triangular shapes of diastolic to systolic transitions. (B,C) BP variations over 10 s (B) and 40 s (C) scale. Vasovagal Response in BP (D) and HR (E) in response to ± 3 mA 0.025 Hz sinusoidal Galvanic Vestibular Stimulation (sGVS). This stimulus (F) generated a VVR, which is characterized by a transient decline in BP (D) followed by a decline in HR (E). The two vertical lines represent the start and stop of stimulation, respectively. The low level of HR outlasted the low level of BP (D,E). There was also a transient drop in BP (G) and HR (H) in response to nose up tilt of 60° (I). The tilt up and back are shown by the two vertical lines, respectively. The transient drops in BP are generally slower than during sGVS, but the recovery follows a similar time course where HR rises to baseline values slower than BP (G,H).
Mentions: The model was derived from data showing that BP is a temporally repetitive waveform that can be analyzed at different time scales. At the smallest time scale (1 s) there are systolic to diastolic transitions whose waveform is approximately triangular in shape and can be reproduced by the relaxation oscillator developed in this study (Figure 1A). The idea that the heart oscillation can be described by a relaxation oscillator was first introduced by Van der Pol and Van der Mark (1928) and models based on this idea are discussed by Noble and Noble (2011). An important point of the model presented here is that the shape of the systolic/diastolic waveform is not determined strictly by the heart. It is determined by an internal model (relaxation oscillator) through a feedback neural network, which mimics the oscillation features of the heart. The feedback mechanisms implement closed loop control and then activate actuators through nonlinear mechanisms that control the constriction of the vascular beds, which has been referred to as peripheral vascular resistance. The feedback from the baroreceptors is compared with the output of the internal model to implement model-reference control. At a larger time scale (10 s), oscillations in systolic amplitude related to breathing can be observed (Figure 1B). There are also small amplitude very low frequency oscillations in the systolic and diastolic BP that have been termed Mayer waves (Mayer, 1876; Myers et al., 2001; Julien, 2006) as well as low frequency oscillations, which are associated with VVR's, which we have termed VasVagal Oscillations (Yakushin et al., 2014).

Bottom Line: Stochastic changes in threshold maintained the compensatory Baroreflex Sensitivity.Sudden decreases in Desired BP elicited non-compensatory VVRs with smaller pulse pressures, consistent with experimental data.It also shows that a VVR is generated when the vestibular input triggers a marked reduction in Desired BP.

View Article: PubMed Central - PubMed

Affiliation: Department of Computer and Information Science, Institute for Neural and Intelligent Systems, Brooklyn College, City University of New York New York, NY, USA.

ABSTRACT
Blood Pressure (BP), comprised of recurrent systoles and diastoles, is controlled by central mechanisms to maintain blood flow. Periodic behavior of BP was modeled to study how peak amplitudes and frequencies of the systoles are modulated by vestibular activation. The model was implemented as a relaxation oscillator, driven by a central signal related to Desired BP. Relaxation oscillations were maintained by a second order system comprising two integrators and a threshold element in the feedback loop. The output signal related to BP was generated as a nonlinear function of the derivative of the first state variable, which is a summation of an input related to Desired BP, feedback from the states, and an input from the vestibular system into one of the feedback loops. This nonlinear function was structured to best simulate the shapes of systoles and diastoles, the relationship between BP and Heart Rate (HR) as well as the amplitude modulations of BP and Pulse Pressure. Increases in threshold in one of the feedback loops produced lower frequencies of HR, but generated large pulse pressures to maintain orthostasis, without generating a VasoVagal Response (VVR). Pulse pressures were considerably smaller in the anesthetized rats than during the simulations, but simulated pulse pressures were lowered by including saturation in the feedback loop. Stochastic changes in threshold maintained the compensatory Baroreflex Sensitivity. Sudden decreases in Desired BP elicited non-compensatory VVRs with smaller pulse pressures, consistent with experimental data. The model suggests that the Vestibular Sympathetic Reflex (VSR) modulates BP and HR of an oscillating system by manipulating parameters of the baroreflex feedback and the signals that maintain the oscillations. It also shows that a VVR is generated when the vestibular input triggers a marked reduction in Desired BP.

No MeSH data available.


Related in: MedlinePlus