scholarly journals Evidence from high-altitude acclimatization for an integrated cerebrovascular and ventilatory hypercapnic response but different responses to hypoxia

2017 ◽  
Vol 123 (6) ◽  
pp. 1477-1486 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Rui Carlos Sá ◽  
Ethan T. Li ◽  
Miriam Scadeng ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Control Mechanism ◽  
Integrated Control ◽  
Acute Hypoxia ◽  
Absolute Value ◽  
Ventilatory Responses ◽  
Two Systems ◽  
Hypercapnic Response ◽  
Sustained Hypoxia

Ventilation and cerebral blood flow (CBF) are both sensitive to hypoxia and hypercapnia. To compare chemosensitivity in these two systems, we made simultaneous measurements of ventilatory and cerebrovascular responses to hypoxia and hypercapnia in 35 normal human subjects before and after acclimatization to hypoxia. Ventilation and CBF were measured during stepwise changes in isocapnic hypoxia and iso-oxic hypercapnia. We used MRI to quantify actual cerebral perfusion. Measurements were repeated after 2 days of acclimatization to hypoxia at 3,800 m altitude (partial pressure of inspired O2 = 90 Torr) to compare plasticity in the chemosensitivity of these two systems. Potential effects of hypoxic and hypercapnic responses on acute mountain sickness (AMS) were assessed also. The pattern of CBF and ventilatory responses to hypercapnia were almost identical. CO2 responses were augmented to a similar degree in both systems by concomitant acute hypoxia or acclimatization to sustained hypoxia. Conversely, the pattern of CBF and ventilatory responses to hypoxia were markedly different. Ventilation showed the well-known increase with acute hypoxia and a progressive decline in absolute value over 25 min of sustained hypoxia. With acclimatization to hypoxia for 2 days, the absolute values of ventilation and O2 sensitivity increased. By contrast, O2 sensitivity of CBF or its absolute value did not change during sustained hypoxia for up to 2 days. The results suggest a common or integrated control mechanism for CBF and ventilation by CO2 but different mechanisms of O2 sensitivity and plasticity between the systems. Ventilatory and cerebrovascular responses were the same for all subjects irrespective of AMS symptoms. NEW & NOTEWORTHY Ventilatory and cerebrovascular hypercapnic response patterns show similar plasticity in CO2 sensitivity following hypoxic acclimatization, suggesting an integrated control mechanism. Conversely, ventilatory and cerebrovascular hypoxic responses differ. Ventilation initially increases but adapts with prolonged hypoxia (hypoxic ventilatory decline), and ventilatory sensitivity increases following acclimatization. In contrast, cerebral blood flow hypoxic sensitivity remains constant over a range of hypoxic stimuli, with no cerebrovascular acclimatization to sustained hypoxia, suggesting different mechanisms for O2 sensitivity in the two systems.

Cerebrovascular and ventilatory responses to acute isocapnic hypoxia in healthy aging and lung disease: effect of vitamin C

2015 ◽  
Vol 119 (4) ◽  
pp. 363-373 ◽  
Author(s):  
Sara E. Hartmann ◽  
Xavier Waltz ◽  
Christine K. Kissel ◽  
Lian Szabo ◽  
Brandie L. Walker ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vitamin C ◽  
Healthy Aging ◽  
Cerebral Blood Flow Velocity ◽  
Acute Hypoxia ◽  
Ventilatory Responses ◽  
Disease Effect ◽  
Effects Of Aging

Acute hypoxia increases cerebral blood flow (CBF) and ventilation (V̇e). It is unknown if these responses are impacted with normal aging, or in patients with enhanced oxidative stress, such as (COPD). The purpose of the study was to 1) investigate the effects of aging and COPD on the cerebrovascular and ventilatory responses to acute hypoxia, and 2) to assess the effect of vitamin C on these responses during hypoxia. In 12 Younger, 14 Older, and 12 COPD, we measured peak cerebral blood flow velocity (V̄p; index of CBF), and V̇e during two 5-min periods of acute isocapnic hypoxia, under conditions of 1) saline-sham; and 2) intravenous vitamin C. Antioxidants [vitamin C, superoxide dismutase (SOD), glutathione peroxidase, and catalase], oxidative stress [malondialdehyde (MDA) and advanced protein oxidation product], and nitric oxide metabolism end products (NOx) were measured in plasma. Following the administration of vitamin C, vitamin C, SOD, catalase, and MDA increased, while NOx decreased. V̄p and V̇e sensitivity to hypoxia was reduced in Older by ∼60% ( P < 0.02). COPD patients exhibited similar V̄p and V̇e responses to Older ( P > 0.05). Vitamin C did not have an effect on the hypoxic V̇e response but selectively decreased the V̄p sensitivity in Younger only. These findings suggest a reduced integrative reflex (i.e., cerebrovascular and ventilatory) during acute hypoxemia in healthy older adults. Vitamin C does not appear to have a large influence on the cerebrovascular or ventilatory responses during acute hypoxia.

scholarly journals Effect of acute hypoxia on regional cerebral blood flow: effect of sympathetic nerve activity

2014 ◽  
Vol 116 (9) ◽  
pp. 1189-1196 ◽  
Author(s):  
Nia C. S. Lewis ◽  
Laura Messinger ◽  
Brad Monteleone ◽  
Philip N. Ainslie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerve ◽  
Regional Difference ◽  
Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Adrenergic Blockade ◽  
Percentage Increase ◽  
Nerve Activity ◽  
Global Cerebral Blood Flow

We examined 1) whether global cerebral blood flow (CBF) would increase across a 6-h bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in the vertebral artery (VA) than in the internal carotid artery (ICA); and 2) whether additional increases in global CBF would be evident following an α1-adrenergic blockade via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA and VA flow were obtained in normoxia (baseline) and following 60, 210, and 330 min of hypoxia (FiO2 = 0.11). Ninety minutes prior to final assessment, participants received an α1-adrenoreceptor blocker (prazosin, 1 mg/20 kg body mass) or placebo. Compared with baseline, following 60, 220, and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow) ∗ 2] increased by 160 ± 52 ml/min (+28%; P = 0.05), 134 ± 23 ml/min (+23%; P = 0.02), and 113 ± 51 (+19%; P = 0.27), respectively. Compared with baseline, ICAFlow increased by 23% following 60 min of hypoxia ( P = 0.06), after which it progressively declined. The percentage increase in VA flow was consistently larger than ICA flow during hypoxia by ∼20% ( P = 0.002). Compared with baseline, ICA and VA diameters increased during hypoxia by ∼9% and ∼12%, respectively ( P ≤ 0.05), and were correlated with reductions in SaO2. Flow and diameters were unaltered following α1 blockade ( P ≥ 0.10). In conclusion, elevations in global CBF during acute hypoxia are partly mediated via greater increases in VA flow compared with ICA flow; this regional difference was unaltered following α1 blockade, indicating that a heightened sympathetic nerve activity with hypoxia does not constrain further dilation of larger extracranial blood vessels.

Fetal cerebral blood flow, electrocorticographic activity, and oxygenation: responses to acute hypoxia

2009 ◽  
Vol 587 (9) ◽  
pp. 2033-2047 ◽  
Author(s):  
S. J. Lee ◽  
D. P. Hatran ◽  
T. Tomimatsu ◽  
J. P. Pena ◽  
G. McAuley ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Hypoxia

scholarly journals Acute hypoxia increases the cerebral metabolic rate – a magnetic resonance imaging study

2015 ◽  
Vol 36 (6) ◽  
pp. 1046-1058 ◽  
Author(s):  
Mark B Vestergaard ◽  
Ulrich Lindberg ◽  
Niels Jacob Aachmann-Andersen ◽  
Kristian Lisbjerg ◽  
Søren Just Christensen ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Oxygen Saturation ◽  
Healthy Subjects ◽  
Acute Hypoxia ◽  
Resonance Imaging ◽  
Cerebral Metabolic Rate

The aim of the present study was to examine changes in cerebral metabolism by magnetic resonance imaging of healthy subjects during inhalation of 10% O2 hypoxic air. Hypoxic exposure elevates cerebral perfusion, but its effect on energy metabolism has been less investigated. Magnetic resonance imaging techniques were used to measure global cerebral blood flow and the venous oxygen saturation in the sagittal sinus. Global cerebral metabolic rate of oxygen was quantified from cerebral blood flow and arteriovenous oxygen saturation difference. Concentrations of lactate, glutamate, N-acetylaspartate, creatine and phosphocreatine were measured in the visual cortex by magnetic resonance spectroscopy. Twenty-three young healthy males were scanned for 60 min during normoxia, followed by 40 min of breathing hypoxic air. Inhalation of hypoxic air resulted in an increase in cerebral blood flow of 15.5% ( p = 0.058), and an increase in cerebral metabolic rate of oxygen of 8.5% ( p = 0.035). Cerebral lactate concentration increased by 180.3% ([Formula: see text]), glutamate increased by 4.7% ([Formula: see text]) and creatine and phosphocreatine decreased by 15.2% ( p[Formula: see text]). The N-acetylaspartate concentration was unchanged ( p = 0.36). In conclusion, acute hypoxia in healthy subjects increased perfusion and metabolic rate, which could represent an increase in neuronal activity. We conclude that marked changes in brain homeostasis occur in the healthy human brain during exposure to acute hypoxia.

scholarly journals Regional cerebral blood flow during acute hypoxia in individuals susceptible to acute mountain sickness

2008 ◽  
Vol 160 (3) ◽  
pp. 267-276 ◽  
Author(s):  
Edward A.W. Dyer ◽  
Susan R. Hopkins ◽  
Joanna E. Perthen ◽  
Richard B. Buxton ◽  
David J. Dubowitz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Regional Cerebral Blood ◽  
Mountain Sickness

scholarly journals Cerebral blood flow changes during intermittent acute hypoxia in patients with heart failure

2018 ◽  
Vol 46 (10) ◽  
pp. 4214-4225 ◽  
Author(s):  
Antonio P. Mansur ◽  
Glaura Souza Alvarenga ◽  
Liliane Kopel ◽  
Marco Antonio Gutierrez ◽  
Fernanda Marciano Consolim-Colombo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Brachial Artery ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Carbon Dioxide Concentration ◽  
Control Group ◽  
Compensatory Mechanisms

Objective Heart failure (HF) is associated with intermittent hypoxia, and the effects of this hypoxia on the cardiovascular system are not well understood. This study was performed to compare the effects of acute hypoxia (10% oxygen) between patients with and without HF. Methods Fourteen patients with chronic HF and 17 matched control subjects were enrolled. Carotid artery changes were examined during the first period of hypoxia, and brachial artery changes were examined during the second period of hypoxia. Data were collected at baseline and after 2 and 4 minutes of hypoxia. Norepinephrine, epinephrine, dopamine, and renin were measured at baseline and after 4 minutes hypoxia. Results The carotid blood flow, carotid systolic diameter, and carotid diastolic diameter increased and the carotid resistance decreased in patients with HF. Hypoxia did not change the carotid compliance, distensibility, brachial artery blood flow and diameter, or concentrations of sympathomimetic amines in patients with HF, but hypoxia increased the norepinephrine level in the control group. Hypoxia increased minute ventilation and decreased the oxygen saturation and end-tidal carbon dioxide concentration in both groups. Conclusion Hypoxia-induced changes in the carotid artery suggest an intensification of compensatory mechanisms for preservation of cerebral blood flow in patients with HF.

White Mountain Expedition 2019: The Impact of Sustained Hypoxia on Cerebral Blood Flow Responses and Tolerance to Simulated Hemorrhage

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Alexander J. Rosenberg ◽  
Garen K. Anderson ◽  
Haley J. Barnes ◽  
Jordan Bird ◽  
Brandon Pentz ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Simulated Hemorrhage ◽  
The Impact ◽  
Sustained Hypoxia

Effects of Alfentanil on the Ventilatory Response to Sustained Hypoxia

1998 ◽  
Vol 89 (3) ◽  
pp. 612-619. ◽  
Author(s):  
Christopher R. Cartwright ◽  
Lindsey C. Henson ◽  
Denham Ward
Keyword(s):  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Initial Increase ◽  
Absolute Value ◽  
Computer Controlled ◽  
The Absolute ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Hypoxia ◽  
Healthy Persons

Background The ventilatory response to acute hypoxia is biphasic, with an initial rapid increase followed by a slower decline. In humans, there is evidence that the magnitude of the decline in ventilation is proportional to the size of the initial increase. This study was done to define the role of exogenous opioids in the ventilatory decline seen with prolonged hypoxia. Methods Ten healthy persons were exposed to isocapnic hypoxia for 25 min, followed by 5 min of isocapnic normoxia and 5 min of isocapnic hypoxia. These conditions were repeated during a computer-controlled alfentanil infusion. Results Serum alfentanil levels were constant among the volunteers (38+/-12 ng/ml). Alfentanil decreased both the initial and second acute hypoxic responses (from 1.27+/-0.73 to 0.99+/-0.39 l x min(-1) x %(-1), P &lt; 0.05; and from 0.99+/-0.70 to 0.41+/-0.29 l x min(-1) x %(-1), P &lt; 0.05, respectively). The magnitude of the decrease in ventilation during the 25 min of hypoxia was not changed (10+/-3.3 l/min for control; 12.3+/-7.5 l/min for alfentanil). Conclusions Alfentanil reduced the acute ventilatory response to hypoxia. The absolute value of hypoxic ventilatory decline was not increased, but a measure of residual hypoxic ventilatory decline (the ratio of ventilation between the second and first steps into hypoxia) was decreased, which supports the hypothesis that opioids potentiate centrally mediated ventilatory decline.

Electroencephalograms and cerebral blood flow in carp, Cyprinus carpio, subjected to acute hypoxia

1995 ◽  
Vol 46 (1) ◽  
pp. 114-122 ◽  
Author(s):  
H. Yoshikawa ◽  
Y. Ishida ◽  
K. Kawata ◽  
F. Kawai ◽  
M. Kanamori
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cyprinus Carpio ◽  
Acute Hypoxia ◽  
Carp Cyprinus Carpio

Ventilatory, cerebrovascular, and cardiovascular interactions in acute hypoxia: regulation by carbon dioxide

2004 ◽  
Vol 97 (1) ◽  
pp. 149-159 ◽  
Author(s):  
Philip N. Ainslie ◽  
Marc J. Poulin
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Blood Flow Velocity ◽  
Acute Hypoxia ◽  
Random Order ◽  
Transcranial Doppler Ultrasound ◽  
Individual Variability ◽  
Cerebral Vasoconstriction ◽  
Arterial Blood ◽  
End Tidal

This study examined the effect of high, normal, and uncontrolled end-tidal Pco2 (PetCO2) on the ventilatory, peak cerebral blood flow velocity ( V̄p), and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, three hypoxic protocols (end-tidal Po2 was held at eight steps between 300 and 45 Torr) in conditions of hypercapnia, isocapnia, or poikilocapnia (PetCO2 +7.5 Torr, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure V̄p in the middle cerebral artery. The slopes of the linear regressions of ventilation, V̄p, and MAP with arterial O2 saturation were significantly greater in hypercapnia than in both isocapnia and poikilocapnia ( P < 0.05). Strong, significant correlations were observed between ventilation, V̄p, and MAP with each PetCO2 condition. These data suggest that 1) a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses during poikilocapnia hypoxia, due to hypocapnic-induced cerebral vasoconstriction; and 2) in hypercapnic hypoxia, a high AHVR is associated with a high acute hypoxic cerebral blood flow response, demonstrating a linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of PetCO2 and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in V̄p and MAP responses to hypoxia. Individuals with a high AHVR are found also to have high V̄p and MAP responses to hypoxia.

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