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.

scholarly journals Cerebral Blood Flow Response to Increases in Arterial CO2 Tension during Alfentanil Anesthesia in the Rabbit

1992 ◽  
Vol 12 (3) ◽  
pp. 529-532 ◽  
Author(s):  
G. L. Ludbrook ◽  
S. C. Helps ◽  
D. F. Gorman
Keyword(s):  
Blood Flow ◽  
Carbon Dioxide Tension ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Cerebral Function ◽  
Cortical Function ◽  
Hydrogen Ion Concentration ◽  
Flow Response ◽  
The Stability ◽  
The Right

The stability of cerebral function and blood flow (CBF), and the CBF response to changes in arterial carbon dioxide tension (CBF reactivity) during alfentanil anesthesia were examined in rabbits. This model was first shown to provide stable anesthesia, cortical function, and CBF for 4 h. CBF increased significantly to 159% [of baseline] in the left hemisphere and to 167% in the right within 5 min of an exposure to 5% CO2 ( p = 0.009 on the left and p = 0.003 on the right), but then decreased to 123% on the left and to 137% on the right (not significantly different from baseline, p = 0.11 on the left and p = 0.07 on the right) while PaCO2 was still rising. Steady state reactivity levels (0.8 ml 100 g−1/min−1/mm Hg−1 CO2 on the left and 0.65 ml 100 g−1/min−1/mm Hg−1 CO2 on the right) were consistent with previous work and were reached at 20 min. These results suggest that mechanisms other than perivascular hydrogen ion concentration mediate the CBF response to changes in arterial CO2 tension during alfentanil anesthesia.

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.

Changes in blood gases and acid-base balance in the exercising dog

1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie
Keyword(s):  
Venous Blood ◽  
Blood Gases ◽  
Respiratory Alkalosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Mixed Venous Blood ◽  
Acid Base Balance ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood ◽  
Mixed Venous

Effects of varying rates of treadmill work on blood gases and hydrogen ion concentrations of four healthy young dogs were determined by analyses of blood for O2 and CO2 contents, Po2, Pco2, and pH. Changes in these parameters were also observed during 30-min recovery periods from hard work. Arterial and mixed venous blood samples were obtained simultaneously during work through a polyethylene catheter in the right ventricle and an indwelling needle in an exteriorized carotid artery. Mixed venous O2 content, Po2 and O2 saturation fell with increased work, whereas arterial values showed little or no change. Mixed venous CO2 content, Pco2, and hydrogen ion concentration exhibited little change from resting levels in two dogs but increased significantly in two others during exercise. These values always decreased in the arterial blood during exercise, indicating the presence of respiratory alkalosis. On cessation of exercise, hyperventilation increased the degree of respiratory alkalosis, causing it to be reflected on the venous side of the circulation. Submitted on January 8, 1962

scholarly journals Mechanisms of Cerebrovascular O2 Sensitivity from Hyperoxia to Moderate Hypoxia in the Rat

1989 ◽  
Vol 9 (2) ◽  
pp. 187-195 ◽  
Author(s):  
Tadashi Shinozuka ◽  
Edwin M. Nemoto ◽  
Peter M. Winter
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Simultaneous Solution ◽  
Hydrogen Ion Concentration ◽  
State Reduction ◽  
Moderate Hypoxia ◽  
Cortical Cerebral Blood Flow ◽  
Tissue Acidosis

Cerebrovascular dilation over PaO2 ranging from hyperoxia to moderate hypoxia is unexplained. We hypothesize that tissue acidosis is the cause. Local cortical cerebral blood flow (LCBF), tissue hydrogen ion concentration [H+]t, and tissue Po2 (Pto2) were measured with microelectrodes in the parietal cortex of 18 rats during a 30-min steady state on 60 to 10% inspired O2 (Pao2, 300 to 40 torr) during 40% N2O analgesia. Five rats kept on 60% O2/40% N2O served as controls. In 18 rats at a Pao2 of 275 ± 7 torr (X̄ ± SEM) and Paco2 of 35 ±1 torr, cerebral values were: LCBF = 129 ± 23 (X̄ ± SEM) ml · 100 g−1 · min−1; [H+], = 62 ± 6 n M; and Pto2 = 25 ± 3 torr. As Pao2 was reduced from about 300 to 40 torr, changes in these variables in percentage of control with respect to Pao2, were described by the following equations, all at P < 0.0001: LCBF = 85.9 + 5,572/Pao2; [H+]t = 97.15 + 1,012/Pao2; and = 108.8 − 3,492/Pao2. Simultaneous solution of the LCBF and [H+]t equations at various Pao2 revealed a slope of 8.82%/n M. Direct correlation between LCBF in ml · 100 g−1 · min−1 and [H+]t in n M revealed a linear relationship defined by the equation Y = − 7.472 + 1.6705 X ( r = 0.6426) for [H+]t between 56 and 160 n M (pH = 7.25 and 6.80) but no correlation at [H+]t values between 56 and 32 n M (pH = 7.25 to 7.50). Cerebrovascular tone is directly correlated with [H+]t during progressive, 30-min steady-state reduction in Pao2 from 350 to 40 torr.

scholarly journals Increased ventilatory response to carbon dioxide in COPD patients following vitamin C administration

2015 ◽  
Vol 1 (1) ◽  
pp. 00017-2015 ◽  
Author(s):  
Sara E. Hartmann ◽  
Christine K. Kissel ◽  
Lian Szabo ◽  
Brandie L. Walker ◽  
Richard Leigh ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vitamin C ◽  
Healthy Subjects ◽  
Ventilatory Response ◽  
Hydrogen Ion Concentration ◽  
Blood Flow Response ◽  
Flow Response ◽  
Copd Patients

Patients with chronic obstructive pulmonary disease (COPD) have decreased ventilatory and cerebrovascular responses to hypercapnia. Antioxidants increase the ventilatory response to hypercapnia in healthy humans. Cerebral blood flow is an important determinant of carbon dioxide/hydrogen ion concentration at the central chemoreceptors and may be affected by antioxidants. It is unknown whether antioxidants can improve the ventilatory and cerebral blood flow response in individuals in whom these are diminished. Thus, we aimed to determine the effect of vitamin C administration on the ventilatory and cerebrovascular responses to hypercapnia during healthy ageing and in COPD.Using transcranial Doppler ultrasound, we measured the ventilatory and cerebral blood flow responses to hyperoxic hypercapnia before and after an intravenous vitamin C infusion in healthy young (Younger) and older (Older) subjects and in moderate COPD.Vitamin C increased the ventilatory response in COPD patients (mean (95% CI) 1.1 (0.9–1.1)versus1.5 (1.1–2.0) L·min−1·mmHg−1, p<0.05) but not inYounger(2.5 (1.9–3.1)versus2.4 (1.9–2.9) L·min−1·mmHg−1, p>0.05) orOlder(1.3 (1.0–1.7)versus1.3 (1.0–1.7) L·min−1·mmHg−1, p>0.05) healthy subjects. Vitamin C did not affect the cerebral blood flow response in the young or older healthy subjects or COPD subjects (p>0.05).Vitamin C increases the ventilatory but not cerebrovascular response to hyperoxic hypercapnia in patients with moderate COPD.

H+ and pCO2 as chemical factors in respiratory and cerebral circulatory control

1961 ◽  
Vol 16 (3) ◽  
pp. 473-484 ◽  
Author(s):  
C. J. Lambertsen ◽  
S. J. G. Semple ◽  
M. G. Smyth ◽  
R. Gelfand
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Flow Index ◽  
Brain Blood Flow ◽  
Hydrogen Ion Concentration ◽  
Blood Ph ◽  
Blood Flow Index ◽  
Respiratory Stimulation

The relationships of changes in respiration and brain blood flow index to alterations in arterial and internal jugular venous blood pCO2, [HCO3-], and pH were studied in normal men. Observations during control of alveolar pCO2, first at 44 and then at 50 mm Hg, represented the effects of CO2 breathing. Intravenous infusion of NaHCO3 solution (ca. 2.4 mEq/kg) while maintaining alveolar pCO2 at 50 mm Hg revealed the responses to a lowering of blood [H+] without concurrent change in arterial or internal jugular venous pCO2. Brain blood flow index varied directly with alteration in blood pCO2 and was unaffected by changes in blood pH not produced by pCO2 change. Respiratory measurements indicated a prominent relationship between respiration and blood hydrogen ion concentration, the reversal of the acidemia normally associated with CO2 administration removing approximately 45% of respiratory stimulation induced by hypercapnia. The remaining 55% of the increased ventilation caused by CO2 breathing was not directly related to changes in arterial or internal jugular venous blood pH or [HCO3-]. The residual respiratory effect of CO2 administration was correlated, not only with alteration of pCO2, but with calculated changes in the pH of cerebrospinal fluid. Thus, the total respiratory stimulation produced by CO2 breathing, and its diminution by bicarbonate infusion, can be quantitatively described either in terms of a single stimulus index, hydrogen ion concentration, or in terms of two factors, pH and pCO2. Choice between single and multiple acid-base factors as indices of chemical stimuli in respiratory control remains arbitrary. However, the discussion re-emphasizes that, while respiratory changes do occur when blood pH is altered without change of blood or central pCO2, comparable stimulant effects of molecular CO2 cannot be demonstrated without somewhere producing concurrent modification of pH. Submitted on August 22, 1960

In vivo cerebrovascular reactivity in Wistar and Fischer 344 rat strains during aging

1993 ◽  
Vol 264 (3) ◽  
pp. H851-H858 ◽  
Author(s):  
I. Lartaud ◽  
L. Bray-des-Boscs ◽  
J. M. Chillon ◽  
J. Atkinson ◽  
C. Capdeville-Atkinson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Frontal Cortex ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Fischer 344 Rats ◽  
Rat Strains ◽  
Fischer 344 ◽  
Fischer 344 Rat

Basal cerebral blood flow (CBF) and CBF regulation after hypercapnia and hypotensive hemorrhage were investigated using H2 clearance in the frontal cortex of awake 2-, 14-, or 23-mo-old Wistar or Fischer 344 rats. Basal CBF decreased in old Wistar but not in mature Wistar (old 64.4 +/- 2.8, mature 87.6 +/- 2.6, young 79.6 +/- 2.2 ml.min-1 x 100 g-1) or in old Fischer 344 (old 71.9 +/- 2.9, young 73.3 +/- 1.6 ml.min-1 x 100 g-1) rats. Cerebrovascular reactivity to hypercapnia decreased in mature and old Wistar (old 2.1 +/- 0.3, mature 3.1 +/- 0.7, young 7.0 +/- 2.1 ml.min-1 x 100 g-1 x mmHg-1) but not in old Fischer 344 rats (old 4.6 +/- 1.4, young 4.9 +/- 0.9 ml.min-1 x 100 g-1 x mmHg-1). The lower limit of CBF autoregulation increased by 20 mmHg during maturation and/or aging in the two strains. Because blood gases and pH evolved similarly in both strains, we postulate that differences in cerebrovascular structure and/or function explain the differences in CBF regulation in the older representatives of the two strains.

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