scholarly journals Prolonged Effects of Cholinesterase Inhibition with Eptastigmine on the Cerebral Blood Flow-Metabolism Ratio of Normal Rats

1993 ◽  
Vol 13 (4) ◽  
pp. 702-711 ◽  
Author(s):  
Oscar U. Scremin ◽  
A. M. Erika Scremin ◽  
Deborah Heuser ◽  
Raymond Hudgell ◽  
Elsa Romero ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Regression Line ◽  
Brain Regions ◽  
Metabolic Effects ◽  
Cholinesterase Inhibition ◽  
Arterial Blood ◽  
A Value ◽  
Similar Dose

The cerebrovascular and metabolic effects of the novel cholinesterase inhibitor eptastigmine were tested in conscious rats. The drug was administered by single intravenous injection, and blood flow or glucose utilization were assessed in 38 brain regions by quantitative autoradiographic techniques. A dose-dependent increase in regional cerebral blood flow (rCBF) was obtained for i.v. doses ranging from 0.5 to 3 mg kg−1. Forty minutes after the dose of 1.5 mg kg−1, average rCBF of the 38 regions studied was (mean ± SD) 2.62 ± 0.62 ml g−1 min−1, a value significantly higher than that of saline-injected controls (1.46 ± 0.26; p < 0.005). In contrast, a similar dose of eptastigmine did not significantly alter regional cerebral glucose utilization (rCGU) (0.90 ± 0.21 μmol g−1 min−1) when compared with saline-injected controls (0.99 ± 0.08 μmol g−1 min−1). A linear correlation between rCBF and rCGU was observed both in saline ( r = 0.871) and eptastigmine ( r = 0.873)-injected animals but the slope of the regression line of rCBF on rCGU was significantly higher (p < 0.01) in the eptastigmine group (2.863 ± 0.266) than in the controls that received saline (1.00 ± 0.094). The cerebral vasodilatation induced by eptastigmine peaked at 40 min after drug administration. No toxic signs were observed at the doses used. Mean arterial blood pressure decreased after 0.5 mg kg−1 (control = 109.3 ± 10.56 mm Hg; eptastigmine = 96.6 ± 8.10 mm Hg) but did not differ from control at the higher doses. It is concluded that eptastigmine induces a long-lasting increase in rCBF and a significant enhancement of the rCBF:rCGU ratio in most regions. The results suggest an important role of endogenous acetylcholine in the control of cerebral perfusion.

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.

Adenosine and cerebral capillary perfusion and blood flow during middle cerebral artery occlusion

1989 ◽  
Vol 257 (5) ◽  
pp. H1656-H1662
Author(s):  
M. Anwar ◽  
H. R. Weiss
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Brain Regions ◽  
Artery Occlusion ◽  
Capillary Perfusion ◽  
Arterial Blood ◽  
Cerebral Artery Occlusion

The effects of adenosine on regional cerebral blood flow and indexes of the total and perfused microvascular bed were studied after 1 h of middle cerebral artery occlusion in the anesthetized rat. Iodo[14C]antipyrine was used to determine cerebral blood flow. Fluorescein isothiocyanate-dextran was used to study the perfused microvasculature, and an alkaline phosphatase stain was used to identify the total bed. Mean arterial blood pressure was significantly reduced by adenosine. Cerebral blood flow increased significantly by 75%, except in the flow-restricted cortex where flow averaged 28 +/- 15 (SD) ml.min-1.100 g-1 in control and 34 +/- 33 ml.min-1.100 g-1 in adenosine-treated animals. No significant regional structural differences were observed within the microvascular beds of the two groups. The percentage of the microvascular volume perfused increased significantly in all brain regions in the adenosine-treated rats, including the flow-restricted cortex. The percent perfused arteriolar volume in the flow-restricted cortex was 30 +/- 12% in control and 95 +/- 3% in adenosine-treated animals. Similar values for the capillary bed were 22 +/- 10% in control and 54 +/- 3% in adenosine-treated rats. These results indicate a maintenance of flow with a reduction in diffusion distances in the flow-restricted cortex after treatment with adenosine.

scholarly journals Postnatal Changes in Local Cerebral Blood Flow Measured by the Quantitative Autoradiographic [14C]Iodoantipyrine Technique in Freely Moving Rats

1989 ◽  
Vol 9 (5) ◽  
pp. 579-588 ◽  
Author(s):  
Astrid Nehlig ◽  
Anne Pereira de Vasconcelos ◽  
Sylvette Boyet
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Regions ◽  
Postnatal Period ◽  
High Rate ◽  
Local Cerebral Blood Flow ◽  
Adult Rat ◽  
Freely Moving Rats ◽  
Freely Moving

The postnatal changes in local cerebral blood flow in freely moving rats were measured by means of the quantitative autoradiographic [14C]iodoantipyrine method. The animals were studied at 10, 14, 17, 21, and 35 days and at the adult stage. At 10 days after birth, rates of blood flow were very low and quite homogeneous in most cerebral structures except in a few posterior areas. From these relatively uniform levels, values of local cerebral blood flow rose notably to reach a peak at 17 days in all brain regions studied. Rates of blood flow decreased between 17 and 21 days after birth and then increased from weaning time to reach the known characteristic distribution of the adult rat. The postnatal evolution of local cerebral blood flow in the rat is in good agreement with previous studies in other species such as dog and humans that also show higher rates of cerebral blood flow and glucose utilization at immature stages. However, in the rat, local cerebral blood flow and local cerebral glucose utilization are not coupled over the whole postnatal period studied, since blood flow rates reach peak values at 17 days whereas glucose utilization remains still quite low at that stage. The high rate of cerebral blood flow in the 17-day-old rat may reflect the energetic and biosynthetic needs of the actively developing brain that are completed by the summation of glucose and ketone body utilization.

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.

scholarly journals Acute Brain Injury Is Associated With Prolonged Suppression of Cerebral Blood Flow Oscillations

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Ryan M Jamiolkowski ◽  
Wesley Baker ◽  
W Andrew Kofke ◽  
Ramani Balu
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Frequency Band ◽  
Prognostic Significance ◽  
Low Frequency ◽  
Brain Regions ◽  
Total Power ◽  
Blood Flow Oscillations ◽  
Arterial Blood

Abstract INTRODUCTION Low-frequency oscillations (LFOs, < 0.1 Hz) in cerebral blood flow (CBF) reflect changes in the coordinated activity of neuronal assemblies. Synchronized LFOs across multiple brain regions can be identified using magnetic resonance imaging to reveal functionally connected networks; however, how LFOs are altered by brain injury is largely unknown. METHODS We quantified changes in LFO magnitude over time in brain-injured patients where CBF was recorded continuously using invasive thermal diffusion flowmetry. Intracranial pressure (ICP), brain tissue oxygen (PbO2), and arterial blood pressure (ABP) were recorded concurrently in all patients. For each epoch of uninterrupted CBF data, the power spectral density within the 0.05 to 0.1 Hz frequency band was calculated. Periods of LFO suppression were defined as occurring when equal to 10% of the total power across all frequencies occurred in the 0.05 to 1 Hz frequency band. Average values of CBF, ICP, PbO2, and ABP were compared between suppressed and nonsuppressed epochs across all patients. RESULTS Twenty-five patients were included in this retrospective observational study. LFO suppression was associated with a lower average CBF (11.3 mL/100 g/min suppressed vs 31.6 mL/100 g/min unsuppressed, P < .0001) and lower average PbO2 (21.6 mm Hg suppressed vs 31.0 mm Hg unsuppressed, P < .0001). In a subset of patients, LFO suppression was associated with intracranial hypertension (ICP 25-60 mm Hg). Patients that regained consciousness and were discharged to acute rehab had a lower median fraction of time spent in the suppressed state (0.03 rehab vs 0.67 death/nursing home, P = .053). CONCLUSION Brain injury is associated with the suppression of low-frequency CBF fluctuations. LFO suppression is associated with periods of physiological distress and may provide a sensitive marker of disrupted brain function. The degree of LFO suppression may have a prognostic significance, and the re-emergence of LFOs after a period of suppression may provide a marker of return of consciousness after coma.

Local Cerebral Blood Flow, Local Cerebral Glucose Utilization, and Flow-Metabolism Coupling during Sevoflurane versus Isoflurane Anesthesia in Rats 

1998 ◽  
Vol 89 (6) ◽  
pp. 1480-1488 ◽  
Author(s):  
Christian Lenz ◽  
Annette Rebel ◽  
Klaus van Ackern ◽  
Wolfgang Kuschinsky ◽  
Klaus F. Waschke
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Regions ◽  
Local Analysis ◽  
Sprague Dawley ◽  
Local Cerebral Blood Flow ◽  
Local Cerebral Glucose Utilization ◽  
Isoflurane Anesthesia ◽  
Cerebral Glucose Utilization

Background Compared to isoflurane, knowledge of local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) during sevoflurane anesthesia is limited. Methods LCGU, LCBF, and their overall means were measured in Sprague-Dawley rats (8 groups, n=6 each) during sevoflurane and isoflurane anesthesia, 1 and 2 MAC, and in conscious control animals (2 groups, n=6 each) using the autoradiographic 2-[14C]deoxy-D-glucose and 4-iodo-N-methyl-[14C]antipyrine methods. Results During anesthesia, mean cerebral glucose utilization was decreased: control, 56+/-5 micronmol x 100 g(-1) x min(-1); 1 MAC isoflurane, 32+/-4 micromol x 100 g(-1) x min(-1) (-43%); 1 MAC sevoflurane, 37+/-5 micromol x 100 g(-1) x min(-1) (-34%); 2 MAC isoflurane, 23+/-3 micromol x 100 g(-1) x min(-1) (-58%); 2 MAC sevoflurane, 23+/-5 micromol x 100 g(-1) x min(-1) (-59%). Local analysis showed a reduction in LCGU in the majority of the 40 brain regions analyzed. Mean cerebral blood flow was increased as follows: control 93+/-8 ml x 100 g(-1) x min(-1); 1 MAC isofurane, 119+/-19 ml x 100 g(-1) x min(-1) (+28%); 1 MAC sevoflurane, 104+/-15 ml x 100 g(-1) x min(-1) (+12%); 2 MAC isoflurane, 149+/-17 ml x 100 g(-1) x min(-1) (+60%); 2 MAC sevoflurane, 118+/-21 ml x 100 g(-1) min(-1) (+27%). LCBF was increased in most brain structures investigated. Correlation coefficients obtained for the relationship between LCGU and LCBF were as follows: control 0.93; 1 MAC isoflurane, 0.89; 2 MAC isoflurane, 0.71; 1 MAC sevoflurane, 0.83; 2 MAC sevoflurane, 0.59). Conclusion Mean and local cerebral blood flows were lower during sevoflurane than during isoflurane anesthesia. This difference cannot be explained by differing changes in glucose utilization because glucose utilization was decreased to the same extent in both groups.

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.

scholarly journals Simultaneous Determination of Regional Cerebral Blood Flow and Blood—Brain Glucose Transport Kinetics in the Gerbil

1983 ◽  
Vol 3 (2) ◽  
pp. 193-199 ◽  
Author(s):  
A. Lorris Betz ◽  
Fausto Iannotti
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Cerebral Blood Flow ◽  
Basal Ganglia ◽  
Glucose Transport ◽  
Blood Glucose Concentration ◽  
Brain Regions ◽  
Brain Glucose ◽  
Arterial Blood ◽  
Half Saturation Constant

Cerebral blood flow (CBF) and unidirectional transport of glucose from blood to brain were measured simultaneously in four brain regions of the pentobarbital-anesthetized gerbil. The method consisted of the intravenous injection of a bolus containing [14C]butanol and [3H]glucose, followed by continuous withdrawal of arterial blood and sampling of brain 25 s later. CBF was lowest in the cerebral cortex (50 ml 100 g−1 min−1), highest in the brainstem (89 ml 100 g−1 min−1), and intermediate in the basal ganglia and cerebellum (66 and 69 ml 100 g−1 min−1, respectively). The kinetics of blood-to-brain glucose transport were measured in animals whose blood glucose concentration had been altered by glucose or insulin injections. The half-saturation constant for glucose transport ( Km) was similar in all brain regions (7.37–8.14 m M), while the maximal rate of transport ( Vmax) was lowest in the cerebral cortex (1.55 μmol g−1 min−1) and significantly higher in the basal ganglia, cerebellum, and brainstem (1.81–2.02 μmol g−1 min−1). These values for CBF and glucose transport are similar to those reported in the literature for other pentobarbital-anesthetized animals. The method provides a simple and rapid technique for determining the effect of ischemia and alterations in CBF on blood-to-brain glucose transport.

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.

Catecholamines and the relationship between cerebral blood flow and glucose use

1986 ◽  
Vol 251 (4) ◽  
pp. H824-H833 ◽  
Author(s):  
U. I. Tuor ◽  
L. Edvinsson ◽  
J. McCulloch
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Moderate Hypertension ◽  
Brain Regions ◽  
Dopamine Infusion ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Bbb Permeability ◽  
The Relationship ◽  
The Brain

The effects of hypertension induced by norepinephrine and dopamine infusion on the relationship between local cerebral blood flow (CBF) and local glucose use (GU) were examined in rats with the use of quantitative autoradiographic techniques. After rats recovered from anesthesia, dopamine or norepinephrine was infused at a rate that ensured moderate hypertension [mean arterial blood pressure (MABP) approximately 150 mmHg]. During dopamine infusion (approximately 200 micrograms X kg-1 X min-1), overall CBF-to-GU ratio throughout the brain was elevated (P less than 0.0001) when compared with saline controls. In contrast, during norepinephrine infusion (approximately 10 micrograms X kg-1 X min-1), the overall CBF-to-GU relationship was not altered significantly. The differential effect of the catecholamines was a consequence of the marked increases in local CBF and moderate decreases in GU observed during dopamine infusion, whereas during norepinephrine administration CBF and GU were not significantly altered in most brain regions. Blood-brain barrier (BBB) permeability was increased during moderate hypertension induced by dopamine and not when induced by norepinephrine. During extreme hypertension (MABP greater than 165 mmHg), heterogeneous increases in CBF and BBB permeability occurred (e.g., in the cerebellum and thalamus). Thus the cerebrovascular response to catecholamine infusion was critically dependent on the agent administered, the level of hypertension achieved, and the brain region examined.

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