Sympathetic modulation of hypercapnic cerebral vasodilation in dogs.

DʼAlecy, Louis G.; Rose, Cynthia J.; Sellers, S. A.

doi:10.1161/01.res.45.6.771

Cited by 25 publications

(10 citation statements)

References 46 publications

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“…Alternatively, there are reports to suggest that sympathetic nerve activity influences cerebrovascular reactivity to CO 2 (19,34). In our study, HR decreased during WI, whereas an increase was observed during LBNP, suggesting alterations in vagal and sympathetic nerve activity.…”

Section: Effect Of Cbv Shifts On the Controller Elementsupporting

confidence: 42%

Manipulation of central blood volume and implications for respiratory control function

Miyamoto

Bailey

Nakahara

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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The respiratory operating point (ventilatory or arterial PCO 2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal PCO 2 (PETCO 2 ) and minute ventilation (V E) [V E ϭ S ϫ (PET CO 2 Ϫ B)], whereas the plant was determined by the hyperbolic relationship between V E and PETCO 2 (PETCO 2 ϭ A/V E ϩ C). Changes in V E at the operating point were not observed under either WI or LBNP conditions despite altered PET CO 2 (P Ͻ 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (PETCO 2 intercept B) rightward and leftward, respectively (P Ͻ 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts. system analysis; respiratory control; central blood volume; head-out water immersion; lower body negative pressure THE RESPIRATORY SYSTEM is an important chemoreflex-feedback control system that maintains arterial PCO 2 (Pa CO 2 ), O 2 , and pH remarkably constant via ventilatory regulation. It can be divided into two subsystems (Fig. 1A): a controller (controlling element) and a plant (controlled element) (5,17,18,21,35,41,45,46).Recently, we have characterized these subsystem elements in an open-loop condition and constructed a respiratory equilibrium diagram to illustrate the mechanisms of respiratory control at rest and during exercise in endurance-trained and untrained subjects (46,48,52). Briefly, the controller element approximates a straight line where minute ventilation (V E) increases as a function of Pa CO 2 . The element can be broadly divided into chemoreflex and nonchemoreflex drives to breathe (39). The plant element approximates a hyperbola with a positive asymptote where Pa CO 2 decreases asymptotically as a function of V E (APPENDIX).Since respiration is determined from an intersection point between these two elements on the respiratory equilibrium diagram (Fig. 1B), quantitative analysis of both subsystems can determine how changes in both the controller and plant elements affect V E or Pa CO 2 (5,6,17,18,41,45,46,48); however, to what extent changes in central blood volume (CBV) influence these variables and thus, by consequence, the operating point (V E or Pa CO 2 response) of the respiratory co...

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Section: Effect Of Cbv Shifts On the Controller Elementsupporting

confidence: 42%

Manipulation of central blood volume and implications for respiratory control function

Miyamoto

Bailey

Nakahara

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…For example, even when cerebrovascular CO 2 reactivity is expressed using cerebrovascular conductance, the potential influence of SNA is important. Some studies have suggested that increases in SNA attenuate the rise in CBF associated with hypercapnia (44,94), whereas others have shown no modulating effect (108,167). More recently, in the highly controlled lamb model, it has been reported that cerebral SNA is withdrawn during rapid-eye-movement (REM) sleep, and, therefore, the CBF response to hypercapnia is augmented (34).…”

Section: Methodological Considerations In the Assessment Of Cerebrovamentioning

confidence: 99%

“…Recently, however, elegant animal studies incorporating continuous recording of SNA in the superior cervical ganglion (35) concluded that SNA directed to cerebral vessels increases with acute hypertension, but not hypotension, suggesting that it serves a protective function for the cerebral microcirculation, and not a regulatory role for maintenance of systemic arterial pressure. In addition to the influence of SNA on CA (143,229), there are reports that sympathetic activity influences the reactivity of CBF to Pa CO 2 (44,94). Thus, although the influence might be regarded as minor, CO 2 -induced elevations in SNA have the potential to affect CBF by direct and indirect mechanisms ( Figs.…”

Section: Regulation Of Cbf With Particular Focus On the Influence Of mentioning

confidence: 99%

Integration of cerebrovascular CO₂reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation

Ainslie¹,

Duffin²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

490

513

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Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO(2) (Pa(CO(2))). This physiological response, termed cerebrovascular CO(2) reactivity, is a vital homeostatic function that helps regulate and maintain central pH and, therefore, affects the respiratory central chemoreceptor stimulus. CBF increases with hypercapnia to wash out CO(2) from brain tissue, thereby attenuating the rise in central Pco(2), whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco(2). Cerebrovascular reactivity and ventilatory response to Pa(CO(2)) are therefore tightly linked, so that the regulation of CBF has an important role in stabilizing breathing during fluctuating levels of chemical stimuli. Indeed, recent reports indicate that cerebrovascular responsiveness to CO(2), primarily via its effects at the level of the central chemoreceptors, is an important determinant of eupneic and hypercapnic ventilatory responsiveness in otherwise healthy humans during wakefulness, sleep, and exercise and at high altitude. In particular, reductions in cerebrovascular responsiveness to CO(2) that provoke an increase in the gain of the chemoreflex control of breathing may underpin breathing instability during central sleep apnea in patients with congestive heart failure and on ascent to high altitude. In this review, we summarize the major factors that regulate CBF to emphasize the integrated mechanisms, in addition to Pa(CO(2)), that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO(2). Next, we provide a detailed update on the integration of the role of cerebrovascular CO(2) reactivity and CBF in regulation of chemoreflex control of breathing in health and disease. Finally, we describe the use of a newly developed steady-state modeling approach to examine the effects of changes in CBF on the chemoreflex control of breathing and suggest avenues for future research.

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“…For example, CBF was reduced with stepwise reductions in arterial pressure after sympathetic and/or parasympathetic denervation in rats, suggesting impaired cerebral autoregulation. 7 In addition, CBF decreased with sympathetic nerve stimulation in rats, 5 dogs, 24 and monkeys, 8 and it increased with parasympathetic nerve stimulation in rats. 5 These data suggest autonomic neural control of the cerebral circulation.…”

Section: Steady-state Autoregulationmentioning

confidence: 97%

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

et al. 2002

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Background-The purpose of the present study was to determine the role of autonomic neural control of dynamic cerebral autoregulation in humans. Methods and Results-We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29Ϯ6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (PϽ0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure. Conclusions-These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to

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Sympathetic modulation of hypercapnic cerebral vasodilation in dogs.

Cited by 25 publications

References 46 publications

Manipulation of central blood volume and implications for respiratory control function

Manipulation of central blood volume and implications for respiratory control function

Integration of cerebrovascular CO₂reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

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Sympathetic modulation of hypercapnic cerebral vasodilation in dogs.

Cited by 25 publications

References 46 publications

Manipulation of central blood volume and implications for respiratory control function

Manipulation of central blood volume and implications for respiratory control function

Integration of cerebrovascular CO2reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

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Integration of cerebrovascular CO₂reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation