Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia

2008 ◽  
Vol 104 (2) ◽  
pp. 490-498 ◽  
Author(s):  
Philip N. Ainslie ◽  
Shigehiko Ogoh ◽  
Katie Burgess ◽  
Leo Celi ◽  
Ken McGrattan ◽  
...  

We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1–2 days after arrival at HA (∼5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (−11 ± 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (−12 ± 3 vs. −5 ± 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low-frequency range, indicating CA impairment; hyperoxia lowered these elevations by ∼50% ( P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.

2010 ◽  
Vol 31 (1) ◽  
pp. 283-292 ◽  
Author(s):  
Ken-Ichi Iwasaki ◽  
Rong Zhang ◽  
Julie H Zuckerman ◽  
Yojiro Ogawa ◽  
Lærke H Hansen ◽  
...  

Cerebral blood flow (CBF) increases and dynamic cerebral autoregulation is impaired by acute hypoxia. We hypothesized that progressive hypocapnia with restoration of arterial oxygen content after altitude acclimatization would normalize CBF and dynamic cerebral autoregulation. To test this hypothesis, dynamic cerebral autoregulation was examined by spectral and transfer function analyses between arterial pressure and CBF velocity variabilities in 11 healthy members of the Danish High-Altitude Research Expedition during normoxia and acute hypoxia (10.5% O2) at sea level, and after acclimatization (for over 1 month at 5,260 m at Chacaltaya, Bolivia). Arterial pressure and CBF velocity in the middle cerebral artery (transcranial Doppler), were recorded on a beat-by-beat basis. Steady-state CBF velocity increased during acute hypoxia, but normalized after acclimatization with partial restoration of SaO2 (acute, 78%±2%; chronic, 89%±1%) and progression of hypocapnia (end-tidal carbon dioxide: acute, 34±2 mm Hg; chronic, 21±1 mm Hg). Coherence (0.40±0.05 Units at normoxia) and transfer function gain (0.77±0.13 cm/s per mm Hg at normoxia) increased, and phase (0.86±0.15 radians at normoxia) decreased significantly in the very-low-frequency range during acute hypoxia (gain, 141%±24%; coherence, 136%±29%; phase, −25%±22%), which persisted after acclimatization (gain, 136%±36%; coherence, 131%±50%; phase, −42%±13%), together indicating impaired dynamic cerebral autoregulation in this frequency range. The similarity between both acute and chronic conditions suggests that dynamic cerebral autoregulation is impaired by hypoxia even after successful acclimatization to an extreme high altitude.


2009 ◽  
Vol 296 (5) ◽  
pp. R1598-R1605 ◽  
Author(s):  
David A. Low ◽  
Jonathan E. Wingo ◽  
David M. Keller ◽  
Scott L. Davis ◽  
Jian Cui ◽  
...  

This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA Vmean), as well as MCA Vmean and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 ± 0.2°C, P < 0.001) conditions. Passive heating reduced MCA Vmean [change (Δ) of 8 ± 8 cm/s, P = 0.01], while blood pressure was maintained (Δ −1 ± 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 ± 0.13 to 0.26 ± 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07–0.20 Hz, P = 0.40) and high-frequency (0.20–0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 ± 0.38 to 0.59 ± 0.19 cm·s−1·mmHg−1, P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 ± 4 mmHg, heat stress: 19 ± 6 mmHg, P = 0.88) and MCA Vmean (13 ± 4 to 12 ± 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 ± 0.22 to 0.38 ± 0.13 ΔCBVC units/s, P = 0.16) and the time for MCA Vmean to recover to precuff deflation baseline (10.0 ± 7.9 to 8.7 ± 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.


2008 ◽  
Vol 109 (4) ◽  
pp. 642-650 ◽  
Author(s):  
Yojiro Ogawa ◽  
Ken-ichi Iwasaki ◽  
Ken Aoki ◽  
Wakako Kojima ◽  
Jitsu Kato ◽  
...  

Background Dexmedetomidine, which is often used in intensive care units in patients with compromised circulation, might induce further severe decreases in cerebral blood flow (CBF) with temporal decreases in arterial pressure induced by various stimuli if dynamic cerebral autoregulation is not improved. Therefore, the authors hypothesized that dexmedetomidine strengthens dynamic cerebral autoregulation. Methods Fourteen healthy male subjects received placebo, low-dose dexmedetomidine (loading, 3 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.2 microg x kg(-1) x h(-1) for 60 min), and high-dose dexmedetomidine (loading, 6 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.4 microg x kg(-1) x h(-1) for 60 min) infusions in a randomized, double-blind, crossover study. After 70 min of drug administration, dynamic cerebral autoregulation was estimated by transfer function analysis between arterial pressure variability and CBF velocity variability, and the thigh cuff method. Results Compared with placebo, steady state CBF velocity and mean blood pressure significantly decreased during administration of dexmedetomidine. Transfer function gain in the very-low-frequency range increased and phase in the low-frequency range decreased significantly, suggesting alterations in dynamic cerebral autoregulation in lower frequency ranges. Moreover, the dynamic rate of regulation and percentage restoration in CBF velocity significantly decreased when a temporal decrease in arterial pressure was induced by thigh cuff release. Conclusion Contrary to the authors' hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.


2016 ◽  
Vol 120 (12) ◽  
pp. 1434-1441 ◽  
Author(s):  
Sung-Moon Jeong ◽  
Seon-Ok Kim ◽  
Darren S. DeLorey ◽  
Tony G. Babb ◽  
Benjamin D. Levine ◽  
...  

Cerebral vasomotor reactivity (CVMR) and dynamic cerebral autoregulation (CA) are measured extensively in clinical and research studies. However, the relationship between these measurements of cerebrovascular function is not well understood. In this study, we measured changes in cerebral blood flow velocity (CBFV) and arterial blood pressure (BP) in response to stepwise increases in inspired CO2 concentrations of 3 and 6% to assess CVMR and dynamic CA in 13 healthy young adults [2 women, 32 ± 9 (SD) yr]. CVMR was assessed as percentage changes in CBFV (CVMRCBFV) or cerebrovascular conductance index (CVCi, CVMRCVCi) in response to hypercapnia. Dynamic CA was estimated by performing transfer function analysis between spontaneous oscillations in BP and CBFV. Steady-state CBFV and CVCi both increased exponentially during hypercapnia; CVMRCBFV and CVMRCVCi were greater at 6% (3.85 ± 0.90 and 2.45 ± 0.79%/mmHg) than at 3% CO2 (2.09 ± 1.47 and 0.21 ± 1.56%/mmHg, P = 0.009 and 0.005, respectively). Furthermore, CVMRCBFV was greater than CVMRCVCi during either 3 or 6% CO2 ( P = 0.017 and P < 0.001, respectively). Transfer function gain and coherence increased in the very low frequency range (0.02-0.07 Hz), and phase decreased in the low-frequency range (0.07–0.20 Hz) when breathing 6%, but not 3% CO2. There were no correlations between the measurements of CVMR and dynamic CA. These findings demonstrated influences of inspired CO2 concentrations on assessment of CVMR and dynamic CA. The lack of correlation between CVMR and dynamic CA suggests that cerebrovascular responses to changes in arterial CO2 and BP are mediated by distinct regulatory mechanisms.


2010 ◽  
Vol 108 (5) ◽  
pp. 1162-1168 ◽  
Author(s):  
Yu-Chieh Tzeng ◽  
Samuel J. E. Lucas ◽  
Greg Atkinson ◽  
Chris K. Willie ◽  
Philip N. Ainslie

The functional relationship between dynamic cerebral autoregulation (CA) and arterial baroreflex sensitivity (BRS) in humans is unknown. Given that adequate cerebral perfusion during normal physiological challenges requires the integrated control of CA and the arterial baroreflex, we hypothesized that between-individual variability in dynamic CA would be related to BRS in humans. We measured R-R interval, blood pressure, and cerebral blood flow velocity (transcranial Doppler) in 19 volunteers. BRS was estimated with the modified Oxford method (nitroprusside-phenylephrine injections) and spontaneous low-frequency (0.04–0.15) α-index. Dynamic CA was quantified using the rate of regulation (RoR) and autoregulatory index (ARI) derived from the thigh-cuff release technique and transfer function analysis of spontaneous oscillations in blood pressure and mean cerebral blood flow velocity. Results show that RoR and ARI were inversely related to nitroprusside BRS [ R = −0.72, confidence interval (CI) −0.89 to −0.40, P = 0.0005 vs. RoR; R = −0.69, CI −0.88 to −0.35, P = 0.001 vs. ARI], phenylephrine BRS ( R = −0.66, CI −0.86 to −0.29, P = 0.0002 vs. RoR; R = −0.71, CI −0.89 to −0.38, P = 0.0001 vs. ARI), and α-index ( R = −0.70, CI −0.89 to −0.40, P = 0.0008 vs. RoR; R = −0.62, CI −0.84 to −0.24, P = 0.005 vs. ARI). Transfer function gain was positively related to nitroprusside BRS ( R = 0.62, CI 0.24–0.84, P = 0.0042), phenylephrine BRS ( R = 0.52, CI 0.10–0.79, P = 0.021), and α-index ( R = 0.69, CI 0.35–0.88, P = 0.001). These findings indicate that individuals with an attenuated dynamic CA have greater BRS (and vice versa), suggesting the presence of possible compensatory interactions between blood pressure and mechanisms of cerebral blood flow control in humans. Such compensatory adjustments may account for the divergent changes in dynamic CA and BRS seen, for example, in chronic hypotension and spontaneous hypertension.


2012 ◽  
Vol 112 (2) ◽  
pp. 266-271 ◽  
Author(s):  
Ken-ichi Iwasaki ◽  
Yojiro Ogawa ◽  
Ken Aoki ◽  
Ryo Yanagida

We examined changes in cerebral circulation in 15 healthy men during exposure to mild +Gz hypergravity (1.5 Gz, head-to-foot) using a short-arm centrifuge. Continuous arterial pressure waveform (tonometry), cerebral blood flow (CBF) velocity in the middle cerebral artery (transcranial Doppler ultrasonography), and partial pressure of end-tidal carbon dioxide (ETco2) were measured in the sitting position (1 Gz) and during 21 min of exposure to mild hypergravity (1.5 Gz). Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis between beat-to-beat mean arterial pressure (MAP) and mean CBF velocity (MCBFV). Steady-state MAP did not change, but MCBFV was significantly reduced with 1.5 Gz (−7%). ETco2 was also reduced (−12%). Variability of MAP increased significantly with 1.5 Gz in low (53%)- and high-frequency ranges (88%), but variability of MCBFV did not change in these frequency ranges, resulting in significant decreases in transfer function gain between MAP and MCBFV (gain in low-frequency range, −17%; gain in high-frequency range, −13%). In contrast, all of these indexes in the very low-frequency range were unchanged. Transfer from arterial pressure oscillations to CBF fluctuations was thus suppressed in low- and high-frequency ranges. These results suggest that steady-state global CBF was reduced, but dynamic cerebral autoregulation in low- and high-frequency ranges was improved with stabilization of CBF fluctuations despite increases in arterial pressure oscillations during mild +Gz hypergravity. We speculate that this improvement in dynamic cerebral autoregulation within these frequency ranges may have been due to compensatory effects against the reduction in steady-state global CBF.


2003 ◽  
Vol 95 (4) ◽  
pp. 1439-1445 ◽  
Author(s):  
William H. Cooke ◽  
Guy L. Pellegrini ◽  
Olga A. Kovalenko

Complete ganglion blockade alters dynamic cerebral autoregulation, suggesting links between systemic autonomic traffic and regulation of cerebral blood flow velocity. We tested the hypothesis that acute head-down tilt, a physiological maneuver that decreases systemic sympathetic activity, would similarly disrupt normal dynamic cerebral autoregulation. We studied 10 healthy young subjects (5 men and 5 women; age 21 ± 0.88 yr, height 169 ± 3.1 cm, and weight 76 ± 6.1 kg). ECG, beat-by-beat arterial pressure, respiratory rate, end-tidal CO2 concentration, and middle cerebral blood flow velocity were recorded continuously while subjects breathed to a metronome. We recorded data during 5-min periods and averaged responses from three Valsalva maneuvers with subjects in both the supine and -10° head-down tilt positions (randomized). Controlled-breathing data were analyzed in the frequency domain with power spectral analysis. The magnitude of input-output relations were determined with cross-spectral techniques. Head-down tilt significantly reduced Valsalva phase IV systolic pressure overshoot from 36 ± 4.0 (supine position) to 25 ± 4.0 mmHg (head down) ( P = 0.03). Systolic arterial pressure spectral power at the low frequency decreased from 5.7 ± 1.6 (supine) to 4.4 ± 1.6 mmHg2 (head down) ( P = 0.02), and mean arterial pressure spectral power at the low frequency decreased from 3.3 ± 0.79 (supine) to 2.0 ± 0.38 mmHg2 (head down) ( P = 0.05). Head-down tilt did not affect cerebral blood flow velocity or the transfer function magnitude and phase angle between arterial pressure and cerebral blood flow velocity. Our results show that in healthy humans, mild physiological manipulation of autonomic activity with acute head-down tilt has no effect on the ability of the cerebral vasculature to regulate flow velocity.


2005 ◽  
Vol 288 (3) ◽  
pp. H1461-H1467 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Mads K. Dalsgaard ◽  
Chie C. Yoshiga ◽  
Ellen A. Dawson ◽  
David M. Keller ◽  
...  

We investigated whether dynamic cerebral autoregulation is affected by exhaustive exercise using transfer-function gain and phase shift between oscillations in mean arterial pressure (MAP) and middle cerebral artery (MCA) mean blood flow velocity ( Vmean). Seven subjects were instrumented with a brachial artery catheter for measurement of MAP and determination of arterial Pco2 (PaCO2) while jugular venous oxygen saturation (SvO2) was determined to assess changes in whole brain blood flow. After a 10-min resting period, the subjects performed dynamic leg-cycle ergometry at 168 ± 5 W (mean ± SE) that was continued to exhaustion with a group average time of 26.8 ± 5.8 min. Despite no significant change in MAP during exercise, MCA Vmean decreased from 70.2 ± 3.6 to 57.4 ± 5.4 cm/s, SvO2 decreased from 68 ± 1 to 58 ± 2% at exhaustion, and both correlated to PaCO2 (5.5 ± 0.2 to 3.9 ± 0.2 kPa; r = 0.47; P = 0.04 and r = 0.74; P < 0.001, respectively). An effect on brain metabolism was indicated by a decrease in the cerebral metabolic ratio of O2 to [glucose + one-half lactate] from 5.6 to 3.8 ( P < 0.05). At the same time, the normalized low-frequency gain between MAP and MCA Vmean was increased ( P < 0.05), whereas the phase shift tended to decrease. These findings suggest that dynamic cerebral autoregulation was impaired by exhaustive exercise despite a hyperventilation-induced reduction in PaCO2.


1998 ◽  
Vol 18 (3) ◽  
pp. 311-318 ◽  
Author(s):  
Terry Bo-Jau Kuo ◽  
Chang-Ming Chern ◽  
Wen-Yung Sheng ◽  
Wen-Jang Wong ◽  
Han-Hwa Hu

We applied frequency domain analysis to detect and quantify spontaneous fluctuations in the blood flow velocity of the middle cerebral artery (MCAFV). Instantaneous MCAFV of normal volunteers was detected using transcranial Doppler sonography. Spectral and transfer function analyses of MCAFV and arterial blood pressure (ABP) were performed by fast Fourier transform. We found the fluctuations in MCAFV, like ABP, could be diffracted into three components at specific frequency ranges, designated as high-frequency (HF, 0.15 to 0.4 Hz), low-frequency (LF, 0.04 to 0.15 Hz), and very low-frequency (VLF, 0.016 to 0.04 Hz) components. The HF and LF components of MCAFV exhibited high coherence with those of ABP, indicating great similarity of MCAFV and ABP fluctuations within the two frequency ranges. However, it was not the case for the VLF component. Transfer function analysis revealed that the ABP-MCAFV phase angle was frequency-dependent in the LF range ( r = −0.79, P < 0.001) but not in the HF range. The time delay between LF fluctuations of ABP and those of MCAFV was evaluated as 2.1 seconds. We conclude that in addition to traditional B-wave equivalents, there are at least two different mechanisms for MCAFV fluctuations: the HF and LF fluctuations of MCAFV are basically secondary to those of ABP, and cerebral autoregulation may operate efficiently in LF rather than HF range. Frequency domain analysis offers an opportunity to explore the nature and underlying mechanism of dynamic regulation in cerebral circulation.


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