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 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 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 The effects of hydrogen ion concentration on the simplest steady-state enzyme systems

1971 ◽  
Vol 123 (3) ◽  
pp. 445-453 ◽  
Author(s):  
P. Ottolenghi
Keyword(s):  
Steady State ◽  
Active Site ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Hydrogen Ion Concentration ◽  
Substrate Complex ◽  
Perturbation Term ◽  
Enzyme Substrate ◽  
Enzyme Systems ◽  
Steady State Kinetics

Laidler (1955) showed that consideration of the effect of pH on enzymic mechanisms that obey steady-state kinetics leads to the inclusion in the equations of a ‘perturbation term’ that can introduce curvature into the Lineweaver–Burk plots. He also stated conditions in which this term vanishes. This term can lead to apparent activation by substrate. Further, several cases are shown in which simplification, but not disappearance, of the perturbation term can lead to linearity of Lineweaver–Burk plots. These cases arise when the ionization of groups at the active site either is unaffected or is completely prevented when the enzyme–substrate complex is formed. It is also shown that V(app.) can vary with pH without a concomitant change in Km(app.) in certain cases that obey steady-state kinetics without implying that Km=Ks. When the perturbation term is significant, Dixon's (1953) rules for the calculation of pK values will not always apply.

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

scholarly journals THE EFFECTS OF CHANGES IN HYDROGEN ION CONCENTRATION ON THE BLOOD FLOW OF MORPHINIZED DOGS

1925 ◽  
Vol 1 (6) ◽  
pp. 547-568 ◽  
Author(s):  
Tinsley Randolph Harrison ◽  
Charles P. Wilson ◽  
Alfred Blalock
Keyword(s):  
Blood Flow ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Hydrogen Ion Concentration

Some Aspects of the Arterial Response to Venous Occlusion in Man

1983 ◽  
Vol 65 (1) ◽  
pp. 1-8 ◽  
Author(s):  
M. A. Ireland ◽  
P. Davies ◽  
W. A. Littler
Keyword(s):  
Blood Flow ◽  
Oxygen Tension ◽  
Venous Blood ◽  
Venous Occlusion ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Biphasic Response ◽  
Hydrogen Ion Concentration ◽  
Autonomic Blockade

1. Plethysmographic blood flow records made after venous occlusion of the forearm showed a biphasic response which was first vasodilator and then vasoconstrictor. 2. The myogenic nature of the vascoconstrictor phase was confirmed in eight subjects after total autonomic blockade with atropine, propranolol, phentolamine and guanethidine. 3. Forearm venous blood demonstrated a rise in hydrogen ion concentration and a fall in oxygen tension during venous occlusion, which may contribute to the vasodilatation phase.

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