Intermittent hypoxia reduces cerebrovascular sensitivity to isocapnic hypoxia in humans

Querido, Jordan S.; Godwin, Jesse; Sheel, A. William

doi:10.1016/j.resp.2007.11.002

Cited by 14 publications

(19 citation statements)

References 43 publications

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“…The change in the cerebrovascular response to submaximal exercise was attributed to hyperventilation induced hypocapnia and an increase in haemoglobin concentration. In contrast, IH protocols similar to ours are typically not accompanied with alterations in haemoglobin (Garcia et al 2000) or ventilation at rest (Foster et al 2005;Querido et al 2008). Also, the hypoxic iterations in IH resemble hypoxia/reoxygenation injury, and can blunt the shear stress-induced vasodilation by reductions in NO bioavailability, resulting in reduced vessel dilation during exercise (Wang et al 2007).…”

Section: Effect Of Ih On Cerebrovascular Regulationmentioning

confidence: 81%

“…Studies in animal and in diseased and healthy humans have shown IH decreases the cerebrovascular sensitivity to acute hypoxia at rest (Phillips et al 2004;Foster et al 2005Foster et al , 2007Querido et al 2008). IH increases oxidative stress, which decreases the bioavailability of nitric oxide (NO), thereby leading to a blunted dilation of cerebral vessels (Lavie 2003;Phillips et al 2004).…”

Section: Introductionmentioning

confidence: 99%

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Effects of intermittent hypoxia on the cerebrovascular responses to submaximal exercise in humans

et al. 2008

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Intermittent hypoxia (IH) has been shown to alter the ventilatory and cardiovascular responses to submaximal exercise; however, the effect of IH on the cerebral blood flow (CBF) response to submaximal exercise has not been determined. This study tested the hypothesis that IH would blunt the CBF response during eucapnic and hypercapnic exercise. Nine healthy males underwent 10 consecutive days of isocapnic IH (oxyhaemoglobin saturation = 80%, 1 h day(-1)). Ventilatory, cardiovascular, and cerebrovascular responses to cycle exercise (50, 100, and 150 W) were measured before and after IH. Carbon dioxide (5% CO(2)), a mediator of CBF during exercise, was administered for 2 min of each exercise stage. Over the 10 days of IH, there was an increase in minute ventilation [Formula: see text] during the IH exposures (P < 0.05). Although exercise produced increases in [Formula: see text] middle cerebral artery mean velocity (MCA V (mean)), and mean arterial pressure (P < 0.05), there was no effect of IH. Similarly, hypercapnic exercise increased [Formula: see text] and MCA V (mean) (P < 0.05); however, the magnitude of the response was unchanged following IH. Our findings indicate that ten daily hypoxia exposures does not alter the CBF response to submaximal exercise.

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Section: Effect Of Ih On Cerebrovascular Regulationmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Effects of intermittent hypoxia on the cerebrovascular responses to submaximal exercise in humans

et al. 2008

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“…This response time falls within the time scale of previously reported cerebrovascular and physiological oxygenation responses to ventilatory challenges. In fact, it was reported that cerebral blood flow increased almost immediately after the application of acute isocapnic hypoxia to healthy volunteers [11]. Moreover, the low values of brain PtO 2 induced by hemorrhage in a swine model (PtO 2 decreased from 40 mmHg at baseline to 5 mmHg) were recovered in only ≈ 10 min [14], while brain PtO 2 in rats exhibited a fast response when subjected to changes in the concentration of O 2 and CO 2 in inspired air; the increase in PtO 2 was also CO 2 dose-dependent [10].…”

Section: Discussionmentioning

confidence: 99%

“…Although the changes induced in arterial oxygen saturation (SpO 2 ) by recurrent apneas can be measured by pulse oximetry, we do not know how changes in arterial SpO 2 translate into PtO 2 in brain tissue. In fact, the relationship between these two variables could be modulated by rapid changes in cerebrovascular hemodynamics in response to hypoxia and hypercapnia [9-11]. It could therefore be possible that a physiological response in the cerebral hemodynamics compensates, at least in part, for the reduction in arterial SpO 2 experienced during repeated obstructive events in OSA.…”

Section: Introductionmentioning

confidence: 99%

Changes in oxygen partial pressure of brain tissue in an animal model of obstructive apnea

et al. 2010

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BackgroundCognitive impairment is one of the main consequences of obstructive sleep apnea (OSA) and is usually attributed in part to the oxidative stress caused by intermittent hypoxia in cerebral tissues. The presence of oxygen-reactive species in the brain tissue should be produced by the deoxygenation-reoxygenation cycles which occur at tissue level during recurrent apneic events. However, how changes in arterial blood oxygen saturation (SpO2) during repetitive apneas translate into oxygen partial pressure (PtO2) in brain tissue has not been studied. The objective of this study was to assess whether brain tissue is partially protected from intermittently occurring interruption of O2 supply during recurrent swings in arterial SpO2 in an animal model of OSA.MethodsTwenty-four male Sprague-Dawley rats (300-350 g) were used. Sixteen rats were anesthetized and non-invasively subjected to recurrent obstructive apneas: 60 apneas/h, 15 s each, for 1 h. A control group of 8 rats was instrumented but not subjected to obstructive apneas. PtO2 in the cerebral cortex was measured using a fast-response oxygen microelectrode. SpO2 was measured by pulse oximetry. The time dependence of arterial SpO2 and brain tissue PtO2 was carried out by Friedman repeated measures ANOVA.ResultsArterial SpO2 showed a stable periodic pattern (no significant changes in maximum [95.5 ± 0.5%; m ± SE] and minimum values [83.9 ± 1.3%]). By contrast, brain tissue PtO2 exhibited a different pattern from that of arterial SpO2. The minimum cerebral cortex PtO2 computed during the first apnea (29.6 ± 2.4 mmHg) was significantly lower than baseline PtO2 (39.7 ± 2.9 mmHg; p = 0.011). In contrast to SpO2, the minimum and maximum values of PtO2 gradually increased (p < 0.001) over the course of the 60 min studied. After 60 min, the maximum (51.9 ± 3.9 mmHg) and minimum (43.7 ± 3.8 mmHg) values of PtO2 were significantly greater relative to baseline and the first apnea dip, respectively.ConclusionsThese data suggest that the cerebral cortex is partially protected from intermittently occurring interruption of O2 supply induced by obstructive apneas mimicking OSA.

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“…However, when Ainslie et al 13 evaluated the effect of 12-day cyclic 5-min exposure to 12% O 2 intermittent with 5-min normoxia repeated for 90 min or 12-day continuous hypoxic exposure, they found that CBFV response to poikilocapnic-hypoxia was decreased. Querido et al 7 exposed healthy humans to cyclic IH exposures: six bouts of inhalation of 12% O 2 for 5 min followed by 5-min normoxia daily for 10 days. They found that 10-day IH exposures diminished the isocapnichypoxic stimulated increase in CBFV.…”

Section: Introductionmentioning

confidence: 99%

Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia

Zhang

Shi

Downey

2014

Exp Biol Med (Maywood)

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The effect of moderately extended, intermittent-hypoxia (IH) on cerebral perfusion during changes in CO 2 was unknown. Thus, we assessed the changes in cerebral vascular conductance (CVC) and cerebral tissue oxygenation (ScO 2 ) during experimental hypocapnia and hypercapnia following 14-day normobaric exposures to IH (10% O 2 ). CVC was estimated from the ratio of mean middle cerebral arterial blood flow velocity (transcranial Doppler sonography) to mean arterial pressure (tonometry), and ScO 2 in the prefrontal cortex was monitored by near-infrared spectroscopy. Changes in CVC and ScO 2 during changes in partial pressure of end-tidal CO 2 (P ET CO 2 , mass spectrometry) induced by 30-s paced-hyperventilation (hypocapnia) and during 6-min CO 2 rebreathing (hypercapnia) were compared before and after 14-day IH exposures in eight young nonsmokers. Repetitive IH exposures reduced the ratio of %ÁCVC/ÁP ET CO 2 during hypocapnia (1.00 AE 0.13 vs 1.94 AE 0.35 vs %/mmHg, P ¼ 0.026) and the slope of ÁCVC/ÁP ET CO 2 during hypercapnia (1.79 AE 0.37 vs 2.97 AE 0.64 %/mmHg, P ¼ 0.021), but had no significant effect on ÁScO 2 /ÁP ET CO 2 . The ventilatory response to hypercapnia during CO 2 rebreathing was significantly diminished following 14-day IH exposures (0.83 AE 0.07 vs 1.14 AE 0.09 L/min/mmHg, P ¼ 0.009). We conclude that repetitive normobaric IH exposures significantly diminish variations of cerebral perfusion in response to hypercapnia and hypocapnia without compromising cerebral tissue oxygenation. This IH-induced blunting of cerebral vasoreactivity during CO 2 variations helps buffer excessive oscillations of cerebral underperfusion and overperfusion while sustaining cerebral O 2 homeostasis.

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Intermittent hypoxia reduces cerebrovascular sensitivity to isocapnic hypoxia in humans

Cited by 14 publications

References 43 publications

Effects of intermittent hypoxia on the cerebrovascular responses to submaximal exercise in humans

Effects of intermittent hypoxia on the cerebrovascular responses to submaximal exercise in humans

Changes in oxygen partial pressure of brain tissue in an animal model of obstructive apnea

Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia

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