Internal carotid and vertebral arterial flow velocity in men at high altitude

Huang, Szu-Wei; Moore, Lorna G.; McCullough, R. E.; McCullough, R. G.; Micco, A. J.; Fulco, Charles S.; Cymerman, Allen; Weil, John V.; Reeves, J. T.

doi:10.1152/jappl.1987.63.1.395

Cited by 76 publications

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“…During clamp the identical duration and changes in arterial blood gases were replicated while the subjects breathed. 5,260 m. 10,11,27 Conversely, sea level sensitivity to isocapnic or poikilocapnic hypoxia is greater in the VA. 7,12 Euoxic hypocapnia also elicits greater decreases in VA flow through a broad range of PaCO 2 (~15 to 40 mm Hg); 7 however, this is not a universal finding through smaller changes in PCO 2 . 28 It thus seems that during simultaneous changes in PaO 2 and PaCO 2 , ICA and VA reactivities are similar, as was the case in the present study where ICA and VA showed similar profiles during clamp and apnea.…”

Section: Regulation Of Cerebral Blood Flow During Apneamentioning

confidence: 99%

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Willie

Ainslie

Drviš

et al. 2014

J Cereb Blood Flow Metab

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The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers (n = 17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing ('clamp') was then used to replicate an identical temporal pattern of decreasing arterial PO 2 (PaO 2 ) and increasing arterial PCO 2 (PaCO 2 ) while breathing. End-apnea PaO 2 ranged from 23 to 37 mm Hg (30 ± 7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54 ± 24% versus 34 ± 26%, respectively; however, CBF increased similarly between apnea and clamp (93.6 ± 28% and 83.4 ± 38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

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Section: Regulation Of Cerebral Blood Flow During Apneamentioning

confidence: 99%

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Willie

Ainslie

Drviš

et al. 2014

J Cereb Blood Flow Metab

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“…Studies of cerebral blood flow (CBF) in humans have found increases of about 20 % over the first 2 days of acclimatization to altitude, with subsequent decreases during the following days (Severinghaus, Chiodi, Eger, Brandstater & Hornbein, 1966;Huang, Moore, McCullough, McCullough, Micco, Fulco, Cymerman, Manco-Johnson, Weil & Reeves, 1987). Understanding these changes is complicated by the fact that the hypoxia and hypocapnia of altitude exposure have opposing effects on CBF.…”

Section: Introductionmentioning

confidence: 99%

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Clar

Pedersen²,

Poulin³

et al. 1997

Experimental Physiology

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SUMMARYThis study examines the effects of prolonged hypoxia, with and without control of end-tidal CO2 partial pressure (PET,CO2), on the intensity-weighted mean velocity of blood flow in the middle cerebral artery (VIwM) and on heart rate (HR). Specifically, the time course of the responses, their reversibility with brief periods of hyperoxia and the recovery phase following prolonged hypoxia were all investigated. Twelve subjects were studied, of whom nine provided satisfactory data. A purpose-built chamber was used for the prolonged control of the end-tidal gases, and an end-tidal forcing system was used for generating the brief variations in end-tidal gases. Three 16 h protocols were employed: (1) 8 h eucapnic (average PET,CO, 39 mmHg) hypoxia (end-tidal 02 partial pressure, PETO, = 55 mmHg) followed by 8 h eucapnic euoxia (PETO2 = 100 mmHg); (2) 8 h poikilocapnic (average PET,Co2 4 mmHg below eucapnia) hypoxia (PET,02 = 55 mmHg) followed by 8 h poikilocapnic euoxia (PET,O0 = 100 mmHg); and (3) control (air inspired throughout). VIwM (using Doppler ultrasound) and HR were measured during brief exposures to hypoxic/euoxic and hyperoxic conditions with PET,CO, held 1-2 mmHg above eucapnia, at 0, 20, 240 and 480 min in the first 8 h, and at the same times in the second 8 h. There were no significant trends in VIWM under hypoxic conditions for either hypoxic protocol (ANOVA) and no significant differences between the three protocols for VIwM in hyperoxia (ANOVA). In contrast to VIWM, there was a significant increase in HR over time during both hypoxic exposures (P < 0.01, ANOVA). HR increased to a similar extent for the two types of hypoxia, and there was some suggestion that HR remained elevated after the relief of hypoxia. The results suggest that, with the level of hypoxia employed, progressive changes in HR occur, but that this level and duration of hypoxia has little sustained effect on VIWM.

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“…The general consensus is that upon acute exposure to altitude CBF initially rises and returns to near baseline values within the first few days or 1 -2 weeks of acclimatization (Huang et al, 1987;Jensen et al, 1990;Baumgartner et al, 1994;Lucas et al, 2011;Subudhi et al, 2014). The magnitude in the changes in CBF after altitude exposure depend upon two stimuli with opposing influences on the cerebral circulation: arterial hypoxia and arterial hypocapnia.…”

Section: Discussionmentioning

confidence: 99%

“…The precise pathophysiology of AMS is not known, however, on the basis of early findings increased cerebral blood flow (CBF) in the first few hours of high altitude exposure may play an important role in the pathogenesis of AMS (Huang et al, 1987;Lassen, 1992;Baumgartner et al, 1994). Although early findings indicate that increased CBF is higher in those with AMS than those without AMS symptoms (Baumgartner et al, 1994), this has not been confirmed in later studies (Baumgartner et al, 1999;Dyer et al, 2008;Lucas et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Relationship between Changes in Cerebral Blood Flow with Symptoms of Acute Mountain Sickness in Men Repeatedly Exposed to Simulated High Altitude

Ondrus¹,

Alberty²,

Lyons³

et al. 2017

APE

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Objective: To study the relationship between changes in the cerebral blood flow (CBF) velocity with symptoms of acute mountain sickness (AMS) during simulated high altitude. Research Design and Methods: Mean middle arterial cerebral flow velocity (MCAv) was assessed by transcranial Doppler sonography in 8 healthy lowland male adults aged 20 -24 yrs before and after 6 h and 48 h at simulated altitude corresponding to 4572 m. The same study was repeated three weeks later in the same subjects. End-tidal pCO 2 (ETCO 2 ) and arterial oxygen saturation (SaO 2 ) were measured by standardized procedures. AMS symptoms were recorded using the modified environmental symptoms questionnaire after 6 h and 48 h exposure to calculate the mean score of cerebral (AMS-C) symptoms. Results: Mean MCAv significantly increased with high altitude (HA) by 4% at 6 h HA and 24% at 48 h HA (P < 0.05) compared to sea-level values. We observed a substantial inter-subject variance in MCAv changes, especially in the first hours upon altitude exposure. Within first 2 days, we found a moderate positive correlation between MCAv with decreased ETCO 2 (mean ± SD 32 ± 4 mmHg; r = 0.47, P < 0.05), and a weak negative correlation of MCAv with a similar low SaO 2 (77% ± 8%; r = −0.43, P < 0.05).Five of the 10 original subjects developed symptoms of AMS; however, AMS-C scores decreased (P = 0.08) with increased duration of exposure (6 h HA 0.91 ± 1.09 vs 48 h HA 0.39 ± 0.40). No differences in AMS-C scores were observed when subjects with and without increased MCAv were compared at 6 h HA and 48 h HA. Furthermore, there was no correlation between changes in neither absolute nor relative MCAv and AMS-C scores. Severity of AMS sympHow to cite this paper: Ondruš, P., Alberty, R., Lyons, T., Muza, S., Echavé, V. Our results suggest that there is a lack of relationship between changes in CBF velocity with symptoms of AMS, and that a substantial inter-subject variance exists in the CBF response to high altitude exposure.

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Internal carotid and vertebral arterial flow velocity in men at high altitude

Cited by 76 publications

References 0 publications

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

Relationship between Changes in Cerebral Blood Flow with Symptoms of Acute Mountain Sickness in Men Repeatedly Exposed to Simulated High Altitude

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