Two patterns of daily hypoxic exposure and their effects on measures of chemosensitivity in humans

2007 ◽  
Vol 103 (6) ◽  
pp. 1973-1978 ◽  
Author(s):  
Michael S. Koehle ◽  
A. William Sheel ◽  
William K. Milsom ◽  
Donald C. McKenzie

The purpose of this study was to compare chemoresponses following two different intermittent hypoxia (IH) protocols in humans. Ten men underwent two 7-day courses of poikilocapnic IH. The long-duration IH (LDIH) protocol consisted of daily 60-min exposures to normobaric 12% O2. The short-duration IH (SDIH) protocol comprised twelve 5-min bouts of 12% O2, separated by 5-min bouts of room air, daily. Isocapnic hypoxic ventilatory response (HVR) was measured daily during the protocol and 1 and 7 days following. Hypercapnic ventilatory response (HCVR) and CO2 threshold and sensitivity (by the modified Read rebreathing technique) were measured on days 1, 8, and 14. Following 7 days of IH, the mean HVR was significantly increased from 0.47 ± 0.07 and 0.47 ± 0.08 to 0.70 ± 0.06 and 0.79 ± 0.06 l·min−1·%SaO2−1 (LDIH and SDIH, respectively), where %SaO2 is percent arterial oxygen saturation. The increase in HVR reached a plateau after the third day. One week post-IH, HVR values were unchanged from baseline. HCVR increased from 3.0 ± 0.4 to 4.0 ± 0.5 l·min−1·mmHg−1. In both the hyperoxic and hypoxic modified Read rebreathing tests, the slope of the CO2/ventilation plot was unchanged by either intervention, but the CO2/ventilation curve shifted to the left following IH. There were no correlations between the changes in response to hypoxia and hypercapnia. There were no significant differences between the two IH protocols for any measures, indicating that comparable changes in chemoreflex control occur with either protocol. These results also suggest that the two methods of measuring CO2 response are not completely concordant and that the changes in CO2 control do not correlate with the increase in the HVR.

2001 ◽  
Vol 90 (4) ◽  
pp. 1431-1440 ◽  
Author(s):  
Keisho Katayama ◽  
Yasutake Sato ◽  
Yoshifumi Morotome ◽  
Norihiro Shima ◽  
Koji Ishida ◽  
...  

The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (SaO2 ) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and SaO2 during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (V˙o 2), expired minute ventilation (V˙e), and SaO2 were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2(V˙e/V˙o 2) and SaO2 during submaximal exercise. There were significant correlations among the changes in HVR at rest and inV˙e/V˙o 2 and SaO2 during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.


1995 ◽  
Vol 79 (5) ◽  
pp. 1504-1511 ◽  
Author(s):  
D. Bee ◽  
D. J. Pallot

In a previous study, we showed that the acute hypoxic ventilatory response was blunted in anesthetized chronically hypoxic rats and was restored by blockade of the dopamine D2 receptor with domperidone. We now report observations made during 1–8 days of exposure to 10% O2 on the acute hypoxic ventilatory response and the effect of domperidone and relate them to dopamine content and cellular proliferation in the carotid body. Hypoxic exposure caused a parallel shift in the hypoxic response curve to higher levels of ventilation and arterial oxygen saturation. The greatest response occurred on day 1 and was unaffected by domperidone: dopamine content diminished and mitotic activity increased. By 8 days, hypoxic ventilation approached normal and was significantly augmented by domperidone; in the carotid body, dopamine levels had risen above the control level and mitoses had diminished. Thus the increase in ventilation was inversely related to carotid body dopamine content, which was depressed. The possibility of a causal relationship is discussed.


2011 ◽  
Vol 110 (1) ◽  
pp. 15-28 ◽  
Author(s):  
David G. Gerst ◽  
Sanar S. Yokhana ◽  
Laura M. Carney ◽  
Dorothy S. Lee ◽  
M. Safwan Badr ◽  
...  

This study examined whether time of day and repeated exposure to intermittent hypoxia have an impact on the hypoxic ventilatory response (HVR) and ventilatory long-term facilitation (vLTF). Thirteen participants with sleep apnea were exposed to twelve 4-min episodes of isocapnic hypoxia followed by a 30-min recovery period each day for 10 days. On days 1 (initial day) and 10 (final day) participants completed the protocol in the evening (PM); on the remaining days the protocol was completed in the morning (AM). The HVR was increased in the morning compared with evening on the initial (AM 0.83 ± 0.08 vs. PM 0.64 ± 0.11 l·min−1·%SaO2−1; P ≤ 0.01) and final days (AM 1.0 ± 0.08 vs. PM 0.81 ± 0.09 l·min−1·%SaO2−1; P ≤ 0.01, where %SaO2 refers to percent arterial oxygen saturation). Moreover, the magnitude of the HVR was enhanced following daily exposure to intermittent hypoxia in the morning (initial day 0.83 ± 0.08 vs. final day 1.0 ± 0.08 l·min−1·%SaO2−1; P ≤ 0.03) and evening (initial day 0.64 ± 0.11 vs. final day 0.81 ± 0.09 l·min−1·%SaO2−1; P ≤ 0.03). vLTF was reduced in the morning compared with the evening on the initial (AM 19.03 ± 0.35 vs. PM 22.30 ± 0.49 l/min; P ≤ 0.001) and final (AM 20.54 ± 0.32 vs. PM 23.11 ± 0.54 l/min; P ≤ 0.01) days. Following daily exposure to intermittent hypoxia, vLTF was enhanced in the morning (initial day 19.03 ± 0.35 vs. final day 20.54 ± 0.32 l/min; P ≤ 0.01). We conclude that the HVR is increased while vLTF is decreased in the morning compared with the evening in individuals with sleep apnea and that the magnitudes of these phenomena are enhanced following daily exposure to intermittent hypoxia.


PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 860-864 ◽  
Author(s):  
Sally L. Davidson Ward ◽  
Daisy B. Bautista ◽  
Thomas C. Keens

Failure to arouse in response to hypoxia has been described in infants at increased risk for sudden infant death syndrome (SIDS) and has been suggested as a possible mechanism for SIDS. However, most SIDS victims are not in a high-risk group before death. Thus, if a hypoxic arousal disorder is an important contributor to SIDS, normal infants might fail to arouse from sleep in response to hypoxia. To test this hypothesis, the authors studied hypoxic arousal responses in 18 healthy term infants younger than 7 months of age (age 12.1 ± 1.7 [SEM] weeks; 56% girls). Hypoxic arousal challenges were performed during quiet sleep by rapidly decreasing inspired oxygen tension (Pio2) to 80 mm Hg for 3 minutes or until arousal (eye opening, agitation, and crying) occurred. Tests were performed in duplicate when possible. Only 8 infants (44%) aroused in response to one or more hypoxic challenges; arousal occurred during 8 (32%) of 25 trials. There were no significant differences in lowest Pio2 or arterial oxygen saturation during hypoxia between those infants who aroused and those who failed to arouse. All 18 infants had a fall in their end-tidal carbon dioxide tension during hypoxia, suggesting that each had a hypoxic ventilatory response despite failure to arouse in the majority. Periodic breathing occurred following hypoxia in only 1 (13%) of the 8 trials that resulted in arousal, compared with 16 (94%) of 17 trials without arousal (P < .005). It is concluded that the majority of normal infants younger than 7 months of age fail to arouse from quiet sleep in response to hypoxia, despite the apparent presence of a hypoxic ventilatory response.


1993 ◽  
Vol 75 (3) ◽  
pp. 1117-1122 ◽  
Author(s):  
J. T. Reeves ◽  
R. E. McCullough ◽  
L. G. Moore ◽  
A. Cymerman ◽  
J. V. Weil

There is considerable variation among individuals in the extent of, and the time required for, ventilatory acclimatization to altitude. Factors related to this variation are unclear. The present study tested whether interindividual variation in preascent ventilation or magnitude of hypoxic ventilatory response related to ventilatory acclimatization to altitude. Measurements in 37 healthy resting male subjects at sea level indicated a wide range (34–48 Torr) of end-tidal PCO2 values. When these subjects were taken to Pikes Peak, CO (4,300 m, barometric pressure 462 mmHg), the end-tidal PCO2 values measured on arrival and repeatedly over 19 days were correlated with the sea-level end-tidal PCO2. At 4,300 m, subjects with high end-tidal PCO2 had low values of arterial oxygen saturation (SaO2). Also, sea-level end-tidal PCO2 related to SaO2 after 19 days at 4,300 m. Twenty-six of the subjects had measurements of isocapnic hypoxic ventilatory response (HVR) at sea level. The end-tidal PCO2 values on arrival and after 19 days residence at 4,300 m were inversely related to the sea-level HVR values. Thus both the PCO2 and the HVR as measured at sea level related to the extent of subsequent ventilatory acclimatization (decrease in end-tidal PCO2) and the level of oxygenation at altitude. The finding in our cohort of subjects that sea-level end-tidal PCO2 was inversely related to HVR raised the possibility that among individuals the magnitude of the hypoxic drive to breathe influenced the amount of ventilation at all altitudes, including sea level.


1980 ◽  
Vol 49 (3) ◽  
pp. 374-379 ◽  
Author(s):  
P. H. Hackett ◽  
J. T. Reeves ◽  
C. D. Reeves ◽  
R. F. Grover ◽  
D. Rennie

Sherpas are well known for their physical performance at extreme altitudes, yet they are reported to have blunted ventilatory responses to acute hypoxia and relative hypoventilation in chronic hypoxia. To examine this paradox, we studied ventilatory control in Sherpas in comparison to that in Westerners at both low and high altitude. At low altitude, 25 Sherpas had higher minute ventilation, higher respiratory frequency, and lower end-tidal carbon dioxide tension than 25 Westerners. The hypoxic ventilatory response of Sherpas was found to be similar to that in Westerners, even though long altitude exposure had blunted the responses of some Sherpas. At high altitude, Sherpas again had higher minute ventilation and a tendency toward higher arterial oxygen saturation than Westerners. Oxygen administration increased ventilation further in Sherpas but decreased ventilation in Westerners. We conclude that Sherpas differ from other high-altitude natives; their hypoxic ventilatory response is not blunted, and they exhibit relative hyperventilation.


Author(s):  
Mercedes J. Nagel ◽  
Caitlin P. Jarrard ◽  
Sophie Lalande

Intermittent hypoxia, defined as alternating bouts of breathing hypoxic and normoxic air, has the potential to improve oxygen-carrying capacity through an erythropoietin-mediated increase in hemoglobin mass. The purpose of this study was to determine the effect of a single session of intermittent hypoxia on erythropoietin levels and hemoglobin mass in young healthy individuals. Nineteen participants were randomly assigned to an intermittent hypoxia group (Hyp, n = 10) or an intermittent normoxia group (Norm, n = 9). Intermittent hypoxia consisted of five 4-min hypoxic cycles at a targeted arterial oxygen saturation of 90% interspersed with 4-min normoxic cycles. Erythropoietin levels were measured before and two hours following completion of the protocol. Hemoglobin mass was assessed the day before and seven days after exposure to intermittent hypoxia or normoxia. As expected, the intermittent hypoxia group had a lower arterial oxygen saturation than the intermittent normoxia group during the intervention (Hyp: 89 ± 1 vs. Norm: 99 ± 1%, p < 0.01). Erythropoietin levels did not significantly increase following exposure to intermittent hypoxia (Hyp: 8.2 ± 4.5 to 9.0 ± 4.8, Norm: 8.9 ± 1.7 to 11.1 ± 2.1 mU·mL−1, p = 0.15). Hemoglobin mass did not change following exposure to intermittent hypoxia. This single session of intermittent hypoxia was not sufficient to elicit a significant rise in erythropoietin levels or hemoglobin mass in young healthy individuals.


1994 ◽  
Vol 77 (6) ◽  
pp. 2753-2760 ◽  
Author(s):  
C. E. Elwell ◽  
M. Cope ◽  
A. D. Edwards ◽  
J. S. Wyatt ◽  
D. T. Delpy ◽  
...  

Near-infrared spectroscopy was used to measure global cerebral blood flow and volume in 10 healthy adult volunteers. High- and low-cerebral blood flow compartments were detected with mean flows for all 10 subjects of 59 +/- 21 (SD) and 11 +/- 4 ml.100 g-1.min-1, respectively. The mean cerebral blood volume of the group was 2.85 +/- 0.97 ml/100 g. Analysis of spontaneous changes in the cerebral concentrations of oxyhemoglobin and deoxyhemoglobin demonstrated strong correlations between respiratory rate and the oscillation frequency of cerebral oxyhemoglobin concentration (r = 0.99) and arterial oxygen saturation (SaO2) (r = 0.99). An estimate of the mean cerebral oxygen saturation for all subjects averaged 59.4 +/- 12.4% when their mean SaO2 was 91.8 +/- 2.4% (equivalent to 67.6 +/- 13.8% at a normoxic SaO2 of 98%). These results demonstrate that near-infrared spectroscopy can be used as a noninvasive bedside technique for both qualitative and quantitative evaluation of cerebral hemodynamics and oxygenation in adults.


1989 ◽  
Vol 77 (4) ◽  
pp. 431-437 ◽  
Author(s):  
M. A. A. Airlie ◽  
D. C. Flenley ◽  
P. M. Warren

1. In a double-blind placebo-controlled study, we have investigated the effect of the peripheral chemoreceptor stimulant drug almitrine bismesylate on hypoxic ventilatory drive (expressed as the slope of the minute ventilation/arterial oxygen saturation relationship in litres min−1 %−1) as measured by both progressive isocapnic hypoxia at rest and transient hypoxia (three breaths of 100% N2) during moderate exercise, in seven normal men, to determine if the ventilatory response to the transient hypoxic stimulus is a more specific measure of peripheral chemoreceptor sensitivity to hypoxia. 2. Hypoxic ventilatory drive measured using progressive isocapnic hypoxia ranged from −0.13 to −2.65 litres min−1 % −1 after placebo and from − 0.20 to − 6.48 litres min−1 %−1 after almitrine. The response was greater after almitrine in six of the seven subjects, and the difference was significant for the whole group (P < 0.05). 3. Hypoxic ventilatory drive measured using transient hypoxia ranged from −0.19 to −1.59 litres min−1 %−1 after placebo and from −0.09 to −1.62 litres min−1 %−1 after almitrine. The response was not consistently greater after almitrine, and the difference was not significant for the group. 4. Difficulties in accurately quantifying a brief rise in minute ventilation after transient hypoxia, particularly in subjects with a low hypoxic ventilatory drive, may have masked small changes in the slope of the minute ventilation/arterial oxygen saturation relationship with this method. However, the significant increase in the response to progressive isocapnic hypoxia after almitrine suggests that the failure to demonstrate an effect using transient hypoxic stimuli was not solely due to between-day variation in hypoxic ventilatory drive or the small numbers of subjects studied. 5. We conclude that, although transient hypoxia avoids any central depression of ventilation that might result from the prolonged hypoxia used in the conventional steady state or progressive isocapnic methods (thereby leading to underestimation of the hypoxic ventilatory drive), the ventilatory response to such transient stimuli is also affected by factors other than peripheral chemoreceptor activity.


2020 ◽  
Vol 8 (B) ◽  
pp. 329-333
Author(s):  
Talat Mohammadi ◽  
Hamidreza Jamilian ◽  
Anita Alaghemand ◽  
Alireza Kamali

AIM: The aim of our study was to determine the effect of adjunctive use of dexmedetomidine and metoral with thiopental on hemodynamic status, agitation, patient satisfaction, and duration of seizure in patients with mood disorders in electroconvulsive therapy (ECT). METHODS: This study is a randomized, double-blind, clinical trial. Sixty patients (18–60 years) according to DSM5 criteria had mood disorder and were candidates for ECT. Patients were randomly divided into two groups of 30 each. One group received 5.0 μg/kg dexmedetomidine 10 min before induction of thiopental, and the other group received 5.2 mg intravenous metoprolol immediately before ECT. Patients’ satisfaction, duration of seizure, and arterial oxygen saturation were evaluated. RESULTS: The mean age of both groups was approximately 37 years with the majority of men. No significant difference was found between the two groups in terms of age and sex, blood pressure (BP), heart rate (HR), duration of seizure, and arterial oxygen saturation before ECT. The mean BP and HR in the recovery were lower in the dexmedetomidine group than in the metoral group. Arterial oxygen saturation percentage was not significantly different between the two groups. The recovery time in the dexmedetomidine group was longer than the metoral group (p = 0.001). Post-ECT satisfaction was found to be higher in the dexmedetomidine group than in the metoral group and the mean agitation score was found to be higher in the metoral group. CONCLUSION: Both metoral and dexmedetomidine as adjuvants decrease the hyperdynamic responses of patients after ECT, whereas the effect of dexmedetomidine is more than metoral; on the other hand, neither dexmedetomidine nor metoral has any negative effect on seizure duration, but dexmedetomidine significantly prolonged recovery time as compared to metoral.


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