scholarly journals The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Cerebrovascular Function

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.

scholarly journals REGULATION OF CEREBRAL BLOOD FLOW IN HUMANS: PHYSIOLOGY AND CLINICAL IMPLICATIONS OF AUTOREGULATION

2021 ◽  
Author(s):  
Jurgen A.H.R. Claassen ◽  
Dick H.J. Thijssen ◽  
Ronney B Panerai ◽  
Frank M. Faraci
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Function ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Blood Gases ◽  
Clinical Implications ◽  
Arterial Blood ◽  
The Impact

Brain function critically depends on a close matching between metabolic demands, appropriate delivery of oxygen and nutrients, and removal of cellular waste. This matching requires continuous regulation of cerebral blood flow (CBF), which can be categorized into four broad topics: 1) autoregulation, which describes the response of the cerebrovasculature to changes in perfusion pressure, 2) vascular reactivity to vasoactive stimuli [including carbon dioxide (CO2)], 3) neurovascular coupling (NVC), i.e., the CBF response to local changes in neural activity (often standardized cognitive stimuli in humans), and 4) endothelium-dependent responses. This review focuses primarily on autoregulation and its clinical implications. To place autoregulation in a more precise context, and to better understand integrated approaches in the cerebral circulation, we also briefly address reactivity to CO2 and NVC. In addition to our focus on effects of perfusion pressure (or blood pressure), we describe the impact of select stimuli on regulation of CBF (i.e., arterial blood gases, cerebral metabolism, neural mechanisms, and specific vascular cells), the inter-relationships between these stimuli, and implications for regulation of CBF at the level of large arteries and the microcirculation. We review clinical implications of autoregulation in aging, hypertension, stroke, mild cognitive impairment, anesthesia, and dementias. Finally, we discuss autoregulation in the context of common daily physiological challenges, including changes in posture (e.g., orthostatic hypotension, syncope) and physical activity.

scholarly journals Role of cerebral blood flow in extreme breath holding

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Anthony R. Bain ◽  
Philip N. Ainslie ◽  
Ryan L. Hoiland ◽  
Chris K. Willie ◽  
David B. MacLeod ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oral Administration ◽  
Blood Gases ◽  
Breath Holding ◽  
Breath Hold ◽  
Cyclooxygenase Inhibitor ◽  
Arterial Blood Gases ◽  
Arterial Blood

AbstractThe role of cerebral blood flow (CBF) on a maximal breath-hold (BH) in ultra-elite divers was examined. Divers (n = 7) performed one control BH, and one BH following oral administration of the non-selective cyclooxygenase inhibitor indomethacin (1.2 mg/kg). Arterial blood gases and CBF were measured prior to (baseline), and at BH termination. Compared to control, indomethacin reduced baseline CBF and cerebral delivery of oxygen (CDO

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

scholarly journals Increasing cerebral blood flow reduces the severity of central sleep apnea at high altitude

2018 ◽  
Vol 124 (5) ◽  
pp. 1341-1348 ◽  
Author(s):  
Keith R. Burgess ◽  
Samuel J. E. Lucas ◽  
Katie M. E. Burgess ◽  
Kate E. Sprecher ◽  
Joseph Donnelly ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sleep Apnea ◽  
Healthy Volunteers ◽  
High Altitude ◽  
Ventilatory Response ◽  
Central Sleep Apnea ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Central Chemoreceptors

Earlier studies have indicated an important role for cerebral blood flow in the pathophysiology of central sleep apnea (CSA) at high altitude, but were not decisive. To test the hypothesis that pharmacologically altering cerebral blood flow (CBF) without altering arterial blood gas (ABGs) values would alter the severity of CSA at high altitude, we studied 11 healthy volunteers (8M, 3F; 31 ± 7 yr) in a randomized placebo-controlled single-blind study at 5,050 m in Nepal. CBF was increased by intravenous (iv) acetazolamide (Az; 10 mg/kg) plus intravenous dobutamine (Dob) infusion (2–5 μg·kg−1·min−1) and reduced by oral indomethacin (Indo; 100 mg). ABG samples were collected and ventilatory responses to hypercapnia (HCVR) and hypoxia (HVR) were measured by rebreathing and steady-state techniques before and after drug/placebo. Duplex ultrasound of blood flow in the internal carotid and vertebral arteries was used to measure global CBF. The initial 3–4 h of sleep were recorded by full polysomnography. Intravenous Az + Dob increased global CBF by 37 ± 15% compared with placebo ( P < 0.001), whereas it was reduced by 21 ± 8% by oral Indo ( P < 0.001). ABGs and HVR were unchanged in both interventions. HCVR was reduced by 28% ± 43% ( P = 0.1) during intravenous Az ± Dob administration and was elevated by 23% ± 30% ( P = 0.05) by Indo. During intravenous Az + Dob, the CSA index fell from 140 ± 45 (control night) to 48 ± 37 events/h of sleep ( P < 0.001). Oral Indo had no significant effect on CSA. We conclude that increasing cerebral blood flow reduced the severity of CSA at high altitude; the likely mechanism is via a reduction in the background stimulation of central chemoreceptors.NEW & NOTEWORTHY This work is significant because it shows convincingly for the first time in healthy volunteers that increasing cerebral blood flow will reduce the severity of central sleep apnea in a high-altitude model, without the potentially confounding effects of altering partial pressure of arterial carbon dioxide or the ventilatory response to hypoxia. The proposed mechanism of action is that of increasing the removal of locally produced CO2from the central chemoreceptors, causing the reduction in hypercapnic ventilatory response, hence reducing loop gain.

Effects of experimental fluid-percussion injury of the brain on cerebrovascular reactivity to hypoxia and to hypercapnia

1982 ◽  
Vol 56 (3) ◽  
pp. 332-338 ◽  
Author(s):  
Wlodimierz Lewelt ◽  
Larry W. Jenkins ◽  
J. Douglas Miller
Keyword(s):  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Fluid Percussion Injury ◽  
The Brain ◽  
Experimental Fluid

✓ To test the hypothesis that concussive brain injury interferes with the normal vasodilator response of the cerebral circulation to hypoxemia, 30 cats were subjected to mild (PaO2 50 mm Hg) and severe (PaO2 30 mm Hg) hypoxemia while measurements were made of arterial and intracranial pressure, regional cerebral blood flow (CBF), and arterial blood gases. Ten cats served as controls, 10 were subjected to mild fluid-percussion injury of the brain (0.8 to 1.7 atmospheres (atm)), and 10 to severe injury (2.4 to 4.1 atm). The CBF response to hypercapnia (PaCO2 50 mm Hg) was also tested in most animals, and the response of CBF autoregulation to hemorrhagic hypotension was tested in four animals of each group. Trauma was found to severely attenuate the capacity of CBF to increase during hypoxemia. Responsiveness to hypoxemia appeared to be better preserved in traumatized animals than was autoregulation, but was less robust than the response to hypercapnia.

Arterial blood gases during cardiac arrest: markers of blood flow in a canine model

Resuscitation ◽  
1992 ◽  
Vol 23 (2) ◽  
pp. 101-111 ◽  
Author(s):  
Mark G. Angelos ◽  
Daniel J. DeBehnke ◽  
James E. Leasure
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Blood Gases ◽  
Canine Model ◽  
Arterial Blood Gases ◽  
Arterial Blood

scholarly journals Control of Cerebral Blood Flow by Blood Gases

2021 ◽  
Vol 12 ◽  
Author(s):  
James Duffin ◽  
David J. Mikulis ◽  
Joseph A. Fisher
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Cerebral Blood Flow ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Hydrogen Ion Concentration ◽  
Flow Response ◽  
The Many

Cerebrovascular reactivity can be measured as the cerebrovascular flow response to a hypercapnic challenge. The many faceted responses of cerebral blood flow to combinations of blood gas challenges are mediated by its vasculature’s smooth muscle and can be comprehensively described by a simple mathematical model. The model accounts for the blood flow during hypoxia, anemia, hypocapnia, and hypercapnia. The main hypothetical basis of the model is that these various challenges, singly or in combination, act via a common regulatory pathway: the regulation of intracellular hydrogen ion concentration. This regulation is achieved by membrane transport of strongly dissociated ions to control their intracellular concentrations. The model assumes that smooth muscle vasoconstriction and vasodilation and hence cerebral blood flow, are proportional to the intracellular hydrogen ion concentration. Model predictions of the cerebral blood flow responses to hypoxia, anemia, hypocapnia, and hypercapnia match the form of observed responses, providing some confidence that the theories on which the model is based have some merit.

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