Cerebrospinal fluid production and its relationship to cerebral metabolism and cerebral blood flow

1959 ◽  
Vol 197 (4) ◽  
pp. 825-828 ◽  
Author(s):  
Edgar A. Bering
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Choroid Plexus ◽  
Cerebral Metabolism ◽  
Oxygen Metabolism ◽  
Csf Flow ◽  
Constant Composition ◽  
Fluid Production

The cerebrospinal fluid production has been studied in the dog under conditions of maximum obtainable flow rates from the cisterna magna. Under these conditions the fluid had constant composition and was assumed to represent the cerebrospinal fluid in the intact state. Cerebral blood flow and cerebral oxygen consumption were measured by the method of Kety and Schmidt. The only significant correlations found were with oxygen consumption when the CSF flow rate was in terms of brain weight and with cerebral blood flow and cerebral vascular resistance when CSF flow was in terms of choroid plexus weight. A combined regression equation was calculated which satisfactorily accounted for the observed CSF flow: CSF cu mm/min. = .128 x CMRO2 x brain wgt. + 0.15 x CVR x choroid plexus wt. This suggested separate physiological processes, one correlated with oxygen metabolism and one with hydrodynamic factors of the cerebral blood flow. The data demonstrated that the choroid plexus alone could not have accounted for the entire CSF flow and some must have come from another source, presumably the brain.

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
AM Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Cerebral Circulation ◽  
Brain Metabolism ◽  
Cerebral Metabolism ◽  
Cerebral Oxygen ◽  
Brain Norepinephrine ◽  
Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

Cerebral Blood Flow, Cerebral Metabolism and Cerebrospinal Fluid Biochemistry in Brain-Injured Patients after Exposure to Hyperbaric Oxygen

1976 ◽  
Vol 14 (5) ◽  
pp. 351-364 ◽  
Author(s):  
François Artru ◽  
Bernard Philippon ◽  
Françoise Gau ◽  
Michel Berger ◽  
Raymond Deleuze
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Hyperbaric Oxygen ◽  
Cerebral Metabolism ◽  
Brain Injured ◽  
Injured Patients

Cerebrospinal fluid ionic regulation, cerebral blood flow, and glucose use during chronic metabolic alkalosis

1989 ◽  
Vol 257 (4) ◽  
pp. H1220-H1227 ◽  
Author(s):  
H. Schrock ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Metabolic Alkalosis ◽  
Glucose Utilization ◽  
Cerebral Metabolism ◽  
Brain Structures ◽  
Cerebral Glucose Utilization ◽  
K Concentration ◽  
Low K

Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-[14C]antipyrine and 2-[14C]deoxy-D-glucose method. The treatment induced moderate [15 days, base excess (BE) 16 mM] to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow was detectable in most brain structures when compared with controls. Cerebrospinal fluid (CSF) K+ and H+ concentrations were significantly decreased. During severe hypochloremic alkalosis, cerebral blood flow was decreased by 19% and cerebral glucose utilization by 24% when compared with the control values. The decrease in cerebral blood flow during severe metabolic alkalosis is attributed mainly to the decreased cerebral metabolism and to a lesser extent to a further decrease of the CSF H+ concentration. CSF K+ concentration was not further decreased. The results show an unaltered cerebral blood flow and glucose utilization together with a decrease in CSF H+ and K+ concentrations at moderate metabolic alkalosis and a decrease in cerebral blood flow and glucose utilization together with a further decreased CSF H+ concentration at severe metabolic alkalosis.

scholarly journals Cerebral Blood Flow and Metabolism in Pernicious Anemia

Blood ◽  
1951 ◽  
Vol 6 (3) ◽  
pp. 213-227 ◽  
Author(s):  
PERITZ SCHEINBERG
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Pernicious Anemia ◽  
Vascular Resistance ◽  
Cerebral Metabolism ◽  
Glucose Consumption ◽  
Moderate Increase ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Consumption

Abstract 1. Cerebral blood flow and metabolism were measured in 16 patients with pernicious anemia. Seven of the patients were restudied in various stages of therapy. 2. The patients fell into two equal groups, those with severe anemia and those with moderate or no anemia. In the first group, cerebral blood flow was increased and cerebral vascular resistance decreased; in the second group, cerebal blood flow was decreased and vascular resistance increased. In both groups, cerebral oxygen and glucose consumption was decreased, as was cerebral venous oxygen tension . 3. There was a good correlation between the mental status defects and cerebral oxygen consumption and between severity of neurologic involvement and cerebral oxygen consumption. There was no correlation between cerebro-vascular resistance and cerebral oxygen consumption, nor between degree of anemia and cerebral oxygen consumption. 4. Specific therapy resulted in a moderate increase in cerebral oxygen consumption and cerebro-vascular resistance. In no instance did cerebral oxygen consumption become normal. 5. The disparity between the functional ability of the patients and the low values for cerebral metabolism is discussed. 6. It is concluded that pernicious anemia results in specific nervous system involvement not related to the anemia, and that this damage is at least partially irreversible in many patients.

Abstract 17303: Longitudinal Cerebral Oxygen Metabolism in Congenital Heart Disease

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Jessie Mei Lim ◽  
Davide Marini ◽  
Amandeep Saini ◽  
Stephanie Au-Young ◽  
Steven Fan ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Congenital Heart ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Brain Growth ◽  
Cerebral Oxygen Metabolism ◽  
Cerebral Oxygen Consumption

Background: Brain growth differences are apparent between different types of cyanotic congenital heart disease, but the underlying mechanism remains unclear. Here, we explored and characterized longitudinal cerebral hemodynamic and oxygen metabolism profiles and their relationships to brain growth patterns in infants with single ventricle physiologies (SV) and transposition of the great arteries (TGA). We hypothesized that there are marked differences in cerebral oxygen metabolism in those with SV compared with TGA. Methods: Cerebral blood flow (CBF), oxygen delivery (CDO2) and consumption (CVO2) and brain growth were measured in 103 term newborns with SV and TGA using MRI at pre- and post-surgery and at follow-up. We measured whole brain size by segmenting a 3D steady state free precession acquisition. Cerebral blood flow was measured using phase contrast imaging of the neck vessels and cerebral venous blood oxygen saturation was derived from T2 oximetry of the superior sagittal sinus. TGAs were divided into those with and without ventricular septums. Results: CBF profiles were similar between the 3 lesion groups. Cerebral oxygen delivery trends increased but were not significantly different between cardiac groups. We observed that this may be mediated by different mechanisms: an increase in arterial saturation in TGAs, and an increase in hemoglobin concentration in SVs. Cerebral oxygen consumption in SV infants remained low (p = 0.54) while that of TGA increased over time (TGA IVS p < 0.001; TGA VSD p <0.001) (Fig. 1), mediated by an unchanging oxygen extraction fraction in SVs (p = 0.59). The SV cerebral oxygen consumption profile aligned with their declining brain weight z-score trajectory. Conclusions: In conclusion, there are characteristic differences in hemodynamic adaptations between SVs and TGAs. Changes in oxygen metabolism may be facilitating brain growth trajectories. This informs us of possible mechanisms involved during a time of critical brain development.

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

1975 ◽  
Vol 49 (2) ◽  
pp. 157-169
Author(s):  
N. N. Stanley ◽  
B. G. Salisbury ◽  
L. C. McHenry ◽  
N. S. Cherniack
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Liver Failure ◽  
Metabolic Rate ◽  
Ventilatory Response ◽  
Cerebral Metabolism ◽  
Experimental Production ◽  
Arterial Blood ◽  
Ventilatory Response To Co2

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial Pco2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased Pco2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated Pco2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the Pco2 is increased.

Coupling of Cerebral Blood Flow and Oxygen Metabolism in Infant Pigs during Selective Brain Hypothermia

2000 ◽  
Vol 20 (8) ◽  
pp. 1215-1224 ◽  
Author(s):  
Bernd Walter ◽  
Reinhard Bauer ◽  
Gernot Kuhnen ◽  
Harald Fritz ◽  
Ulrich Zwiener
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Metabolism ◽  
Oxygen Metabolism ◽  
Metabolic Effects ◽  
Main Determinant ◽  
Cerebral Hemodynamic ◽  
Systemic Hypothermia ◽  
C 30 ◽  
The Brain

Studies documenting the cerebral hemodynamic consequences of selective brain hypothermia (SBH) have yielded conflicting data. Therefore, the authors have studied the effect of SBH on the relation of cerebral blood flow (CBF) and CMRO2 in the forebrain of pigs. Selective brain hypothermia was induced in seven juvenile pigs by bicarotid perfusion of the head with extracorporally cooled blood. Cooling and stepwise rewarming of the brain to a Tbrain of 38°C, 25°C, 30°C, and 38°C at normothermic Ttrunk (38°C) decreased CBF from 71 ± 12 mL 100 g−1 min−1 at normothermia to 26 ± 3 mL 100 g−1 min−1 and 40 ± 12 mL 100 g−1 min−1 at a Tbrain of 25°C and 30°C, respectively. The decrease of CMRO2 during cooling of the brain to a Tbrain of 25°C resulted in a mean Q10 of 2.8. The ratio between CBF and CMRO2 was increased at a Tbrain of 25°C indicating a change in coupling of flow and metabolism. Despite this change, regional perfusion remained coupled to regional temperatures during deep cerebral hypothermia. The data demonstrate that SBH decreases CBF and oxygen metabolism to a degree comparable with the cerebrovascular and metabolic effects of systemic hypothermia. The authors conclude that, irrespective of a change in coupling of blood flow and metabolism during deep cerebral hypothermia, cerebral metabolism is a main determinant of CBF during SBH.

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