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.

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.

Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats

1993 ◽  
Vol 265 (4) ◽  
pp. H1243-H1248 ◽  
Author(s):  
K. Waschke ◽  
H. Schrock ◽  
D. M. Albrecht ◽  
K. van Ackern ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Structures ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Conscious Rats ◽  
Cerebral Glucose Utilization ◽  
Arterial Blood ◽  
Blood Exchange

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

Local Coupling of Cerebral Blood Flow to Cerebral Glucose Metabolism during Inhalational Anesthesia in Rats 

1999 ◽  
Vol 91 (6) ◽  
pp. 1720-1720 ◽  
Author(s):  
Christian Lenz ◽  
Thomas Frietsch ◽  
Carsten Fütterer ◽  
Annette Rebel ◽  
Klaus van Ackern ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Structures ◽  
Volatile Anesthetics ◽  
Brain Regions ◽  
Local Analysis ◽  
Sprague Dawley ◽  
Mean Values ◽  
Cerebral Glucose Utilization

Background It is not known whether the effects of desflurane on local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) are different from those of other volatile anesthetics. Methods Using the autoradiographic iodoantipyrine and deoxyglucose methods, LCGU, LCBF, and their overall means were measured in 60 Sprague-Dawley rats (10 groups, n = 6 each) during desflurane and isoflurane anesthesia and in conscious controls. Results During anesthesia, mean cerebral glucose utilization was decreased compared with conscious controls: 1 minimum alveolar concentration (MAC) desflurane: -52%; 1 MAC isoflurane: -44%; 2 MAC desflurane: -62%; and 2 MAC isoflurane: -60%. Local analysis showed a reduction of LCGU in the majority of the 40 brain regions analyzed. Mean cerebral blood flow was increased: 1 MAC desflurane: +40%; 1 MAC isoflurane: +43%; 2 MAC desflurane and 2 MAC isoflurane: +70%. LCBF was increased in all brain structures investigated except in the auditory cortex. No significant differences (P &lt; 0.05) could be observed between both anesthetics for mean values of cerebral glucose use and blood flow. Correlation coefficients obtained for the relation between LCGU and LCBF were as follows: controls: 0.95; 1 MAC desflurane: 0.89; 2 MAC desflurane: 0.60; 1 MAC isoflurane: 0.87; and 2 MAC isoflurane: 0.68. Conclusion Differences in the physicochemical properties of desflurane compared with isoflurane are not associated with major differences in the effects of both volatile anesthetics on cerebral glucose utilization, blood flow, and the coupling between LCBF and LCGU.

Local cerebral glucose utilization and blood flow during metabolic acidosis

1981 ◽  
Vol 241 (5) ◽  
pp. H772-H777 ◽  
Author(s):  
W. Kuschinsky ◽  
S. Suda ◽  
L. Sokoloff
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Acidosis ◽  
Glucose Utilization ◽  
Local Level ◽  
Brain Structures ◽  
Coupling Mechanism ◽  
Tight Coupling ◽  
Local Cerebral Glucose Utilization ◽  
Cerebral Glucose Utilization

The relationship between local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) was studied in two groups of normal conscious rats. LCGU was measured by the [14C]deoxyglucose technique and LCBF by the [14C]iodoantipyrine technique. When the LCGU of 39 brain structures was correlated with their respective values of LCBF an excellent correlation (r = 0.96) was obtained between LCGU and LCBF, demonstrating a tight coupling at a local level. Chronic metabolic acidosis was induced in two other groups of rats by adding 0.35 M NH4Cl to the drinking water for 5-6 days. This resulted in a significant (P less than 0.01) reduction in overall cerebral glucose utilization (-29%) and a nonsignificant reduction in overall cerebral blood flow (-8%). This dissociation between the overall cerebral glucose utilization and blood flow during metabolic acidosis cannot be taken as an indicator of uncoupling because the values for LCGU were still well correlated (r = 0.95) with the values for LCBF, indicating a resetting of the coupling mechanism to a new level.

Effects of Xenon on Cerebral Blood Flow and Cerebral Glucose Utilization in Rats

2001 ◽  
Vol 94 (2) ◽  
pp. 290-297 ◽  
Author(s):  
Thomas Frietsch ◽  
Ralph Bogdanski ◽  
Manfred Blobner ◽  
Christian Werner ◽  
Wolfgang Kuschinsky ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Steady State ◽  
Glucose Utilization ◽  
Brain Structures ◽  
Brain Regions ◽  
Local Cerebral Blood Flow ◽  
Mean Values ◽  
Cerebral Glucose Utilization ◽  
Local Brain

Background The effects of xenon inhalation on mean and local cerebral blood flow (CBF) and mean and local cerebral glucose utilization (CGU) were investigated using iodo-[14C]antipyrine and [14C]deoxyglucose autoradiography. Methods Rats were randomly assigned to the following groups: conscious controls (n = 12); 30% (n = 12) or 70% xenon (n = 12) for 45 min for the measurement of local CBF and CGU; or 70% xenon for 2 min (n = 6) or 5 min (n = 6) for the measurement of local CBF only. Results Compared with conscious controls, steady state inhalation of 30 or 70% xenon did not result in changes of either local or mean CBF. However, mean CBF increased by 48 and 37% after 2 and 5 min of 70% xenon short inhalation, which was entirely caused by an increased local CBF in cortical brain regions. Mean CGU determined during steady state 30 or 70% xenon inhalation remained unchanged, although local CGU decreased in 7 (30% xenon) and 18 (70% xenon) of the 40 examined brain regions. The correlation between CBF and CGU in 40 local brain structures was maintained during steady state inhalation of both 30 and 70% xenon inhalation, although at an increased slope at 70% xenon. Conclusion Effects of 70% xenon inhalation on CBF in rats are time-dependent. During steady state xenon inhalation (45 min), mean values of CBF and CGU do not differ from control values, and the relation of regional CBF to CGU is maintained, although reset at a higher level.

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

Local cerebral circulatory and metabolic effects of indomethacin

1982 ◽  
Vol 243 (3) ◽  
pp. H416-H423 ◽  
Author(s):  
J. McCulloch ◽  
P. A. Kelly ◽  
J. J. Grome ◽  
J. D. Pickard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Metabolic Effects ◽  
Local Cerebral Glucose Utilization ◽  
Synthesis Inhibitor ◽  
Cerebral Glucose Utilization ◽  
The Central Nervous System ◽  
Prostaglandin Synthesis Inhibitor ◽  
Tracer Molecules

The effects of indomethacin, a prostaglandin synthesis inhibitor, upon local cerebral glucose utilization and local cerebral blood flow have been examined in 36 conscious, lightly restrained rats. Cerebral glucose utilization and cerebral blood flow were determined by means of the quantitative autoradiographic techniques that utilize, respectively, 2-deoxy-D-[1-14C]glucose and iodo[14C]antipyrine as tracer molecules. The administration of indomethacin (0.3-30 mg/kg iv) did not alter significantly the rate of glucose utilization in any of the 38 discrete regions of the central nervous system that were examined. In contrast, cerebral blood flow in every region was significantly reduced by between 30 and 50% from vehicle-injected control levels after the administration of 10 mg/kg iv indomethacin and by 5-31% after 1 mg/kg iv indomethacin. These results provide further evidence that prostaglandins may play a major role in cerebrovascular regulation, but they provide no positive evidence for a role in neuronal activity, as reflected in local cerebral glucose utilization.

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