scholarly journals Impaired Dynamic Cerebral Autoregulation at Extreme High Altitude Even after Acclimatization

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.

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.


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.


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.


2021 ◽  
Vol 320 (1) ◽  
pp. R69-R79
Author(s):  
Hayato Tsukamoto ◽  
Aya Ishibashi ◽  
Christopher J. Marley ◽  
Yasushi Shinohara ◽  
Soichi Ando ◽  
...  

We examined the acute impact of both low- and high-glycemic index (GI) breakfasts on plasma brain-derived neurotrophic factor (BDNF) and dynamic cerebral autoregulation (dCA) compared with breakfast omission. Ten healthy men (age 24 ± 1 yr) performed three trials in a randomized crossover order; omission and Low-GI (GI = 40) and High-GI (GI = 71) breakfast conditions. Middle cerebral artery velocity (transcranial Doppler ultrasonography) and arterial pressure (finger photoplethysmography) were continuously measured for 5 min before and 120 min following breakfast consumption to determine dCA using transfer function analysis. After these measurements of dCA, venous blood samples for the assessment of plasma BDNF were obtained. Moreover, blood glucose was measured before breakfast and every 30 min thereafter. The area under the curve of 2 h postprandial blood glucose in the High-GI trial was higher than the Low-GI trial ( P < 0.01). The GI of the breakfast did not affect BDNF. In addition, both very-low (VLF) and low-frequency (LF) transfer function phase or gains were not changed during the omission trial. In contrast, LF gain (High-GI P < 0.05) and normalized gain (Low-GI P < 0.05) were decreased by both GI trials, while a decrease in VLF phase was observed in only the High-GI trial ( P < 0.05). These findings indicate that breakfast consumption augmented dCA in the LF range but High-GI breakfast attenuated cerebral blood flow regulation against slow change (i.e., the VLF range) in arterial pressure. Thus we propose that breakfast and glycemic control may be an important strategy to optimize cerebrovascular health.


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.


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.


1998 ◽  
Vol 274 (1) ◽  
pp. H233-H241 ◽  
Author(s):  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
Cole A. Giller ◽  
Benjamin D. Levine

To test the hypothesis that spontaneous changes in cerebral blood flow are primarily induced by changes in arterial pressure and that cerebral autoregulation is a frequency-dependent phenomenon, we measured mean arterial pressure in the finger and mean blood flow velocity in the middle cerebral artery (V˙MCA) during supine rest and acute hypotension induced by thigh cuff deflation in 10 healthy subjects. Transfer function gain, phase, and coherence function between changes in arterial pressure andV˙MCA were estimated using the Welch method. The impulse response function, calculated as the inverse Fourier transform of this transfer function, enabled the calculation of transient changes inV˙MCA during acute hypotension, which was compared with the directly measured change in V˙MCA during thigh cuff deflation. Beat-to-beat changes inV˙MCA occurred simultaneously with changes in arterial pressure, and the autospectrum of V˙MCA showed characteristics similar to arterial pressure. Transfer gain increased substantially with increasing frequency from 0.07 to 0.20 Hz in association with a gradual decrease in phase. The coherence function was >0.5 in the frequency range of 0.07–0.30 Hz and <0.5 at <0.07 Hz. Furthermore, the predicted change inV˙MCA was similar to the measuredV˙MCA during thigh cuff deflation. These data suggest that spontaneous changes inV˙MCA that occur at the frequency range of 0.07–0.30 Hz are related strongly to changes in arterial pressure and, furthermore, that short-term regulation of cerebral blood flow in response to changes in arterial pressure can be modeled by a transfer function with the quality of a high-pass filter in the frequency range of 0.07–0.30 Hz.


Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Varun Reddy ◽  
Fadar Otite ◽  
Ajit Puri ◽  
Amir Zamani ◽  
Jorge Serrador ◽  
...  

Introduction: We have previously shown that early impairments in dynamic cerebral autoregulation are strongly associated with subsequent development of angiographic cerebral vasospasm. While angiographic cerebral vasospasm is associated with delayed cerebral ischemia (DCI), the relationship between cerebral autoregulation and DCI has not been previously investigated. Our study is designed to specifically test the relationship between early changes in dynamic cerebral autoregulation and subsequent development of DCI. Methods: Thirty-nine consecutive patients with acute non-traumatic subarachnoid hemorrhage (SAH) and adequate transcranial Doppler windows, presenting within 24 hours of symptom onset, have been prospectively studied so far. Daily 5-minute measures of continuous beat-to-beat bilateral middle cerebral artery (MCA) flow velocity and mean arterial blood pressure (MAP) recordings were obtained on days 1-10. Transfer function analysis of spontaneous MAP and MCA mean flow velocity (MFV) oscillations were performed in the very low (0.03-0.07 Hz), low (0.07-0.15 Hz), and high (0.15-0.3 Hz) frequency ranges. Non contrast head CTs were reviewed by a neurologist and neuroradiologist blinded to the autoregulatory and angiographic data. Infarctions present within 6 weeks after SAH, which could not be attributed to instrumentation or peri-op strokes, were identified as DCI. Results: Patients with DCI had significantly higher Hunt and Hess (H&H) scores (median=4 vs 3, p<0.0001) compared to those without DCI. There was no difference in MAP (p=0.746), right MCA (p=0.8327)) or left MCA MFV (p=0.4278) between patients with and without DCI across all time points. Patients with DCI had a lower transfer function phase in the very low frequency (autoregulatory frequency) range. Subgroup analysis of patients with H&H scores ≥3 (N=14) showed that those with DCI had significantly lower phases on day 3 compared to those without DCI (-13±80 vs. 63±26, p=0.048). Conclusion: Our preliminary data show that dynamic cerebral autoregulation, as measured by transfer function phase in the autoregulatory frequency range, is significantly impaired in the early days after SAH and that this early impairment is associated with the development of DCI. We are continuing to collect data on additional patients with SAH to confirm our findings in a larger cohort. Impairments in dynamic cerebral in the early days post SAH may be reliable predictors for identifying patients at higher risk of delayed cerebral ischemia.


2020 ◽  
Vol 120 (12) ◽  
pp. 2693-2704
Author(s):  
Erika Schagatay ◽  
Alexander Lunde ◽  
Simon Nilsson ◽  
Oscar Palm ◽  
Angelica Lodin-Sundström

Abstract Purpose Hypoxia and exercise are known to separately trigger spleen contraction, leading to release of stored erythrocytes. We studied spleen volume and hemoglobin concentration (Hb) during rest and exercise at three altitudes. Methods Eleven healthy lowlanders did a 5-min modified Harvard step test at 1370, 3700 and 4200 m altitude. Spleen volume was measured via ultrasonic imaging and capillary Hb with Hemocue during rest and after the step test, and arterial oxygen saturation (SaO2), heart rate (HR), expiratory CO2 (ETCO2) and respiratory rate (RR) across the test. Results Resting spleen volume was reduced with increasing altitude and further reduced with exercise at all altitudes. Mean (SE) baseline spleen volume at 1370 m was 252 (20) mL and after exercise, it was 199 (15) mL (P < 0.01). At 3700 m, baseline spleen volume was 231 (22) mL and after exercise 166 (12) mL (P < 0.05). At 4200 m baseline volume was 210 (23) mL and after exercise 172 (20) mL (P < 0.05). After 10 min, spleen volume increased to baseline at all altitudes (NS). Baseline Hb increased with altitude from 138.9 (6.1) g/L at 1370 m, to 141.2 (4.1) at 3700 m and 152.4 (4.0) at 4200 m (P < 0.01). At all altitudes Hb increased from baseline during exercise to 146.8 (5.7) g/L at 1370 m, 150.4 (3.8) g/L at 3700 m and 157.3 (3.8) g/L at 4200 m (all P < 0.05 from baseline). Hb had returned to baseline after 10 min rest at all altitudes (NS). The spleen-derived Hb elevation during exercise was smaller at 4200 m compared to 3700 m (P < 0.05). Cardiorespiratory variables were also affected by altitude during both rest and exercise. Conclusions The spleen contracts and mobilizes stored red blood cells during rest at high altitude and contracts further during exercise, to increase oxygen delivery to tissues during acute hypoxia. The attenuated Hb response to exercise at the highest altitude is likely due to the greater recruitment of the spleen reserve during rest, and that maximal spleen contraction is reached with exercise.


2009 ◽  
Vol 107 (4) ◽  
pp. 1165-1171 ◽  
Author(s):  
Andrew W. Subudhi ◽  
Ronney B. Panerai ◽  
Robert C. Roach

We investigated the effect of acute hypoxia (AH) on dynamic cerebral autoregulation (CA) using two independent assessment techniques to clarify previous, conflicting reports. Twelve healthy volunteers (6 men, 6 women) performed six classic leg cuff tests, three breathing normoxic (FiO2 = 0.21) and three breathing hypoxic (FiO2 = 0.12) gas, using a single blinded, Latin squares design with 5-min washout between trials. Continuous measurements of middle cerebral artery blood flow velocity (CBFv; DWL MultiDop X2) and radial artery blood pressure (ABP; Colin 7000) were recorded in the supine position during a single experimental session. Autoregulation index (ARI) scores were calculated using the model of Tiecks et al. (Tiecks FP, Lam AM, Aaslid R, Newell DW. Stroke 26: 1014–1019, 1995) from ABP and CBFv changes following rapid cuff deflation (cuff ARI) and from ABP to CBFv transfer function, impulse, and step responses (TFA ARI) obtained during a 4-min period prior to cuff inflation. A new measure of %CBFv recovery 4 s after peak impulse was also derived from TFA. AH reduced cuff ARI (5.65 ± 0.70 to 5.01 ± 0.96, P = 0.04), TFA ARI (4.37 ± 0.76 to 3.73 ± 0.71, P = 0.04), and %Recovery (62.2 ± 10.9% to 50.8 ± 9.9%, P = 0.03). Slight differences between TFA and cuff ARI values may be attributed to heightened sympathetic activity during cuff tests as well as differential sensitivity to low- and high-frequency components of CA. Together, results provide consistent evidence that CA is impaired with AH. In addition, these findings demonstrate the potential utility of TFA ARI and %Recovery scores for future CA investigations.


Sign in / Sign up

Export Citation Format

Share Document