Arterial Pco2 and cerebral hemodynamics

1964 ◽  
Vol 206 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Martin Reivich
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Full Range ◽  
Cerebral Hemodynamics ◽  
Similar Data ◽  
Cerebral Vasculature ◽  
Arterial Pco2 ◽  
Blood Flows ◽  
Cerebrovascular Resistance ◽  
Blood Temperature

The effect of arterial Pco2 in the control of cerebral hemodynamics over the full range of responsiveness of the cerebral vasculature was studied in the rhesus monkey. Cerebral perfusion pressure and arterial O2 saturation were controlled so that they produced no significant effect on the cerebral circulation. Other possible sources of error, e.g., blood temperature, effect of anesthesia, development of metabolic acidosis, and validity of internal jugular measurements of cerebral blood flow were evaluated. Arterial Pco2 was varied from 5 to 418 mm Hg in eight animals. The minimum and maximum cerebral blood flows obtained were 18 and 140 ml/min 100 g, respectively. These values were approached when the arterial Pco2 was in the range of 10–15 mm Hg and 150 mm Hg, respectively. At these levels of arterial Pco2 the maximum and minimum cerebrovascular resistance occurred. These values were 4.78 and 0.63 mm Hg/ml/min per 100 g, respectively. A mathematical analysis of the data enabled equations relating arterial Pco2 to cerebrovascular resistance and to cerebral blood flow to be derived. Values predicted by these equations compare favorably with the actual measured data and with similar data in the literature.

The effects of graded experimental trauma on cerebral blood flow and responsiveness to CO2

1979 ◽  
Vol 51 (1) ◽  
pp. 18-26 ◽  
Author(s):  
Myles L. Saunders ◽  
J. Douglas Miller ◽  
Donald Stablein ◽  
Gilbert Allen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Severe Trauma ◽  
Cerebrovascular Reactivity ◽  
Cerebral Injury ◽  
Content Type ◽  
Blood Flows ◽  
Cerebrovascular Resistance ◽  
End Tidal ◽  
The Brain

✓ The effects of graded mechanical cerebral trauma on cerebrovascular reactivity to CO2 was studied in 26 cats. A fluid-wave percussion model was employed which delivered an epidural trauma of fixed duration and variable amplitude. The animals were maintained at arterial normoxia, with constant monitoring of intracranial and systemic arterial pressures, electroencephalograms, and end-tidal CO2. Following trauma, cerebral blood flow was measured using the H2 ion clearance technique at PaCO2 levels ranging sequentially from 20 to 60 mm Hg. Cerebrovascular reactivity for control animals (uninjured) was 2.7%. In the group with mild trauma (0.76 to 1.90 atm) reactivity was impaired (1.7%), and it was abolished in the severely injured group (2.90 to 4.60 atm). Mild injuries did not alter resting blood flows, while severe trauma resulted in a significant decrease in cerebrovascular resistance. Intracranial and systemic arterial pressures were altered proportionately to the level of cerebral injury. The authors propose that trauma to the brain-stem vasoregulatory centers accounts for these findings.

scholarly journals Cerebral blood flow velocities and cerebrovascular resistance in normal-term neonates in the first 72 hours

2017 ◽  
Vol 54 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Danielle E Forster ◽  
Emmanuel Koumoundouros ◽  
Virginia Saxton ◽  
Gabrielle Fedai ◽  
James Holberton
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Term Neonates ◽  
Cerebrovascular Resistance ◽  
Normal Term ◽  
Blood Flow Velocities ◽  
Flow Velocities

Dynamics of cerebral blood flow regulation explained using a lumped parameter model

2002 ◽  
Vol 282 (2) ◽  
pp. R611-R622 ◽  
Author(s):  
Mette S. Olufsen ◽  
Ali Nadim ◽  
Lewis A. Lipsitz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cardiovascular Response ◽  
Lumped Parameter Model ◽  
Initial Increase ◽  
Windkessel Model ◽  
Cerebrovascular Resistance ◽  
Posture Change ◽  
Lumped Parameter ◽  
Young Subjects

The dynamic cerebral blood flow response to sudden hypotension during posture change is poorly understood. To better understand the cardiovascular response to hypotension, we used a windkessel model with two resistors and a capacitor to reproduce beat-to-beat changes in middle cerebral artery blood flow velocity (transcranial Doppler measurements) in response to arterial pressure changes measured in the finger (Finapres). The resistors represent lumped systemic and peripheral resistances in the cerebral vasculature, whereas the capacitor represents a lumped systemic compliance. Ten healthy young subjects were studied during posture change from sitting to standing. Dynamic variations of the peripheral and systemic resistances were extracted from the data on a beat-to-beat basis. The model shows an initial increase, followed approximately 10 s later by a decline in cerebrovascular resistance. The model also suggests that the initial increase in cerebrovascular resistance can explain the widening of the cerebral blood flow pulse observed in young subjects. This biphasic change in cerebrovascular resistance is consistent with an initial vasoconstriction, followed by cerebral autoregulatory vasodilation.

Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model

1998 ◽  
Vol 274 (5) ◽  
pp. H1715-H1728 ◽  
Author(s):  
Mauro Ursino ◽  
Carlo Alberto Lodi
Keyword(s):  
Mathematical Model ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Nonlinear Interaction ◽  
Cerebral Blood Volume ◽  
Cerebral Hemodynamics ◽  
Pial Arteries ◽  
Arterial Circulation ◽  
Neurosurgical Patients

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

In Reply: Cerebral Blood Flow

PEDIATRICS ◽  
1982 ◽  
Vol 70 (6) ◽  
pp. 1013-1014
Author(s):  
RAUL BEJAR
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Gastrointestinal Tract ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Left Ventricular Output ◽  
Patent Ductus

Baylen and Emmanouilides give the impression that their abstract was misquoted in our commentary. We would like to explain our interpretation of their data. In the abstract, Baylen et al indicate that they measured regional blood flows (RBF) in premature fetal lambs, expressing them as a percentage of the left ventricular output (LVO) before and after patent ductus arteriosus (PDA) closure. Their results (percent of LVO) before and after PDA closure were: lung, 42.7% vs 8.4% (P < .01); carcass, 35% vs 55% (P < .01); heart, 5.5% vs 10.2% (P < .05); gastrointestinal tract, 5.1% vs 9.3% (P < .05); brain, 2.7% vs 3.4% (P = NS); kidney, 2.2% vs 3.3% (P = NS); liver, 3.2% vs 5.7% (P = NS).

Cerebral blood flow, glucose use, and CSF ionic regulation in potassium-depleted rats

1988 ◽  
Vol 254 (2) ◽  
pp. H250-H257
Author(s):  
H. Schrock ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Local Cerebral Blood Flow ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
K Concentration ◽  
Low K ◽  
The Brain ◽  
K Depletion

Rats were kept on a low-K+ diet for 25 or 70 days. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 31 different structures of the brain by means of the [14C]iodoantipyrine and [14C]2-deoxy-D-glucose method. After 25 and 70 days of K+ depletion LCBF was decreased significantly in 27 and 30 structures, respectively, the average decrease being 19 and 25%. In contrast, average LCGU was not changed. Cisternal cerebrospinal fluid (CSF) K+ concentration decreased significantly from 2.65 +/- 0.02 mM in controls to 2.55 +/- 0.02 mM and 2.47 +/- 0.02 mM in the two treated groups (P less than 0.01). CSF [HCO3-], pH, and PCO2 were increased in K+-depleted animals. These data show that K+ depletion induces an increase in CSF pH and a decrease in CSF K+ concentration, both of which cause a reduction in cerebral blood flow. The increased CSF PCO2 is secondary to the reduction of blood flow, since brain metabolism and arterial PCO2 remained constant.

Effects of hypercapnia on uterine and umbilical circulations in conscious pregnant sheep

1976 ◽  
Vol 41 (5) ◽  
pp. 727-733 ◽  
Author(s):  
A. M. Walker ◽  
G. K. Oakes ◽  
R. Ehrenkranz ◽  
M. McLaughlin ◽  
R. A. Chez
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Co2 Concentration ◽  
Arterial Pco2 ◽  
Physiological Regulation ◽  
Blood Flows ◽  
Umbilical Blood ◽  
Pregnant Sheep ◽  
Near Term ◽  
Vascular Catheters

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2–16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100–200 mg/kg. Mean fetal arterial Pco2 increased from49.5 to 63.4 mmHg but no significant changes in umbilical blood flowoccurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. Nodignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despitean increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistancedid not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor innormal physiological regulation of the uteroplacental circulation in this species.

Accuracy of methods for calculating cerebral blood flow from intracarotid xenon-133 injection

1980 ◽  
Vol 238 (5) ◽  
pp. H750-H758
Author(s):  
J. P. Marc-Vergnes ◽  
P. Celsis ◽  
J. P. Charlet ◽  
G. Setien
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Gray Matter ◽  
Relative Weight ◽  
Compartmental Analysis ◽  
Optimization Method ◽  
Initial Slope ◽  
Method Of Calculation ◽  
Blood Flows ◽  
Xenon 133

The accuracy of the three commonly used methods, the initial slope analysis, the stochastic analysis, and the compartmental analysis, for calculating mean cerebral blood flow from xenon-133 clearance curves was studied with the use of computer-generated and real curves. The accuracy of calculation was affected by the cutoff time of the curve, by the level of the compartmental blood flows to white and gray matter and by the ratio of these flow levels, by the relative weight of gray matter, and by the choice of the method of calculation. None of the methods was clearly superior to the others. Each had its own defects that render it more or less suitable for different situations. All three methods generally overestimated mean cerebral blood flow. This overestimation was greater the lower the flow. A curve-fitting index was devised which can be used to check the validity of the bicompartmental model when using compartmental analysis. This same index can provide, though not always, an estimate of the error in the calculation of mean cerebral blood flow when an optimization method is used.

Sympathetic regulation of cerebral blood flow during seizures in newborn lambs

1988 ◽  
Vol 255 (3) ◽  
pp. H563-H568
Author(s):  
C. D. Kurth ◽  
L. C. Wagerle ◽  
M. Delivoria-Papadopoulos
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Cerebral Blood Flow ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerves ◽  
The Other ◽  
Cerebral White Matter ◽  
Blood Flows ◽  
Sympathetic Regulation ◽  
Sympathetic Nervous

We examined cerebral blood flow (CBF) regulation by the sympathetic nerves in 12 newborn lambs (3–11 days old) during seizures, a potent reflex stimulator of the sympathetic nervous system. CBF was measured with microspheres, and seizures were induced with bicuculline. In six of these lambs, one hemibrain was denervated (D) chronically by interrupting the ipsilateral cervical sympathetic trunk; the other hemibrain remained innervated (I). Before and after 10, 35, and 70 min of seizures, cerebral gray matter blood flow (mean +/- SE ml.min-1.100 g-1) was, respectively, 12 +/- 3 (9%), 71 +/- 12 (21%), 120 +/- 15 (38%), and 54 +/- 5 (14%) greater (P less than 0.05) in the D than in the I hemibrain. In the cerebral white matter, hippocampus, caudate, and thalamus blood flows to the D and I hemibrains were similar before seizures but during seizures they were 10–39% greater (P less than 0.05) in the D than in the I hemibrain. Midbrain, brainstem, and cerebellum D and I blood flows were always similar. In the other six lambs, acute denervation during seizures increased ipsilateral cerebral gray and hippocampus blood flow by 10–31%, but unilateral electrical stimulation decreased ipsilateral cerebral gray, cerebral white, hippocampus, thalamus, and caudate blood flow by 17–27%. The data demonstrate that, during seizures, sympathetic nerve activity modifies regional CBF and the effect is sustained, suggesting a role for the sympathetic nervous system in newborn CBF regulation.

Effect of arterial carbon dioxide on cerebral blood flow in ducks

1977 ◽  
Vol 232 (6) ◽  
pp. H596-H601 ◽  
Author(s):  
B. Grubb ◽  
C. D. Mills ◽  
J. M. Colacino ◽  
K. Schmidt-Nielsen
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Slow Component ◽  
Avian Brain ◽  
Arterial Pco2 ◽  
Pekin Ducks ◽  
Two Component ◽  
Xenon 133

The purpose of this study was to determine the effect of arterial PCO2 on blood flow to the avian brain. Cerebral blood flow was measured on curarized, artificially ventilated Pekin ducks by the rate at which intra-arterially injected xenon-133 was cleared from the duck's brain. A two-component clearance curve resulted: the blood flow calculated from the fast and slow components was similar to the blood flow to mammalian grey and white matter, respectively. Hypercapnia markedly increased the fast component of blood flow, whereas hypocapnia had no effect on this component. These effects were not due to changes in blood pressure, which was independent of arterial PCO2. Blood flow calculated from the slow component was independent of arterial PCO2. We conclude that the lack of response to hypocapnia may contribute to the exceptional tolerance of birds to high altitude by maintaining normal cerebral blood flow.

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