scholarly journals Brain and Blood Concentrations of Propofol after Rapid Intravenous Injection in Sheep, and Their Relationships to Cerebral Effects

1996 ◽  
Vol 24 (4) ◽  
pp. 445-452 ◽  
Author(s):  
G. L. Ludbrook ◽  
R. N. Upton ◽  
C. Grant ◽  
E. C. Gray
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intravenous Injection ◽  
Time Course ◽  
Pharmacokinetic Analysis ◽  
Depth Of Anaesthesia ◽  
Blood Concentrations ◽  
Arterial Blood ◽  
Close Relationship ◽  
The Brain

The time-course of propofol concentrations in the blood and brain following rapid administration of three doses were examined using a sheep preparation and regional pharmacokinetic techniques. These were compared to the time-course of cerebral effects of propofol reported previously. There were marked differences between the time-course of propofol concentrations in arterial blood and the brain, with a close relationship between the time-course of brain concentrations and effects on depth of anaesthesia and CBF. There was evidence that the effect of propofol on cerebral blood flow altered its own rate of elution from the brain. Hysteresis between arterial propofol concentrations and cerebral effects following rapid IV administration therefore appears to have a pharmacokinetic basis, and conventional compartmental pharmacokinetic analysis using blood concentrations alone may fail to accurately predict the time-course of both brain propofol concentrations and depth of anaesthesia.

scholarly journals Measurement of Local Cerebral Blood Flow with [14C]Iodoantipyrine in the Mouse

1988 ◽  
Vol 8 (1) ◽  
pp. 121-129 ◽  
Author(s):  
Therese M. Jay ◽  
Giovanni Lucignani ◽  
Alison M. Crane ◽  
Jane Jehle ◽  
Louis Sokoloff
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Local Cerebral Blood Flow ◽  
Sources Of Error ◽  
Arterial Blood ◽  
Appropriate Care ◽  
Rapid Removal ◽  
The Brain

Local cerebral blood flow was measured in the mouse by means of the [14C]iodoantipyrine method. This method has been previously used in the monkey, dog, cat, and rat, but its application to small mammals such as the mouse requires special attention to potential sources of error. The small size of the mouse brain requires special attention to the rapid removal and freezing of the brain to minimize effects of postmortem diffusion of tracer in the tissue. Because of the relatively low diameter/length ratios of the catheters needed for arterial sampling in small animals, substantial errors can occur in the determination of the time course of the [14C]iodoantipyrine concentration in the arterial blood unless corrections for lag time and dead space washout in the catheter are properly applied. Local cerebral blood flow was measured in seven awake mice with appropriate care to minimize these sources of error. The values were found to vary from 48 ml/100 g/min in the corpus callosum to 198 ml/100 g/min in the inferior colliculus. The results demonstrate that the [14C]iodoantipyrine method can be used to measure local cerebral blood flow in the mouse and that the values in that species are, in general, somewhat higher than those in the rat.

scholarly journals Use of 19F NMR Spectroscopy for Measurement of Cerebral Blood Flow: A Comparative Study Using Microspheres

1989 ◽  
Vol 9 (6) ◽  
pp. 886-891 ◽  
Author(s):  
David Barranco ◽  
Leslie N. Sutton ◽  
Sandra Florin ◽  
Joel Greenberg ◽  
Teresa Sinnwell ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood ◽  
Radioactive Microsphere ◽  
Low Concentrations ◽  
Cat Brain ◽  
Nmr Techniques ◽  
High Concentrations ◽  
Washout Curves ◽  
The Brain

19F NMR was used to determine washout curves of an inert, diffusible gas (CHF3) from the cat brain. The cerebral blood flow was estimated from a bi- or tri-phasic fit to the deconvoluted wash-out curve, using the Kety-Schmidt approach. Cerebral blood flow values determined by 19F NMR show the expected responsiveness to alterations in Paco2, but are approximately 28% lower than cerebral blood flow values determined simultaneously by radioactive microsphere techniques. High concentrations of CHF3 have little effect on intracranial pressure, mean arterial blood pressure or Paco2, but cause small changes in the blood flow to certain regions of the brain. We conclude that 19F NMR techniques utilizing low concentrations of CHF3 have potential for the noninvasive measurement of cerebral blood flow.

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

Autoregulation of cerebral blood flow after experimental fluid percussion injury of the brain

1980 ◽  
Vol 53 (4) ◽  
pp. 500-511 ◽  
Author(s):  
W. Lewelt ◽  
L. W. Jenkins ◽  
J. Douglas Miller
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Injury ◽  
Content Type ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Fluid Percussion Injury ◽  
The Brain

✓ To test the hypothesis that concussive brain injury impairs autoregulation of cerebral blood flow (CBF), 24 cats were subjected to hemorrhagic hypotension in 10-mm Hg increments while measurements were made of arterial and intracranial pressure, CBF, and arterial blood gases. Eight cats served as controls, while eight were subjected to mild fluid percussion injury of the brain (1.5 to 2.2 atmospheres) and eight to severe injury (2.8 to 4.8 atmospheres). Injury produced only transient changes in arterial and intracranial pressure, and no change in resting CBF. Impairment of autoregulation was found in injured animals, more pronounced in the severe-injury group. This could not be explained on the basis of intracranial hypertension, hypoxemia, hypercarbia, or brain damage localized to the area of the blood flow electrodes. It is, therefore, concluded that concussive brain injury produces a generalized loss of autoregulation for at least several hours following injury.

Cerebral Blood Flow in the Rat

1958 ◽  
Vol 193 (2) ◽  
pp. 272-274 ◽  
Author(s):  
Leo A. Sapirstein ◽  
Gordon E. Hanusek
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Intravenous Injection ◽  
Extraction Ratio ◽  
Female Rats ◽  
Perfusion Rate ◽  
Single Intravenous Injection ◽  
The Brain ◽  
Fractional Uptake

The cerebral uptake of iodoantipyrine (I131) was measured in anesthetized rats as a function of time after a single intravenous injection. The cerebral content stabilized in 7–9 seconds and remained constant for 64 seconds indicating that the brain and body had the same extraction ratio for the label. The cerebral blood flow fraction therefore corresponded to the fractional uptake of iodoantipyrine by the brain. The cerebral blood flow was calculated as the product of the cardiac output and the cerebral flow fraction. The perfusion rate of the brain was found to be 0.51 ml/gm/min. in female rats.

Blood-brain barrier permeability of 11C-labeled alcohols and 15O-labeled water

1976 ◽  
Vol 230 (2) ◽  
pp. 543-552 ◽  
Author(s):  
ME Raichle ◽  
JO Eichling ◽  
MG Straatmann ◽  
MJ Welch ◽  
KB Larson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Brain Capillary ◽  
Permeability Characteristics ◽  
Permeability Surface ◽  
Brain Barrier Permeability ◽  
The Individual ◽  
The Brain

The extraction of 11C-labeled methanol, ethanol, and isopropanol, as well as 15O-labeled water by the brain during a single capillary transit, was studied in vivo in six adult rhesus monkeys by external detection of the time course of these tracers subsequent to their internal carotid artery injection. The data demonstrate the feasibility of accurately measuring brain permeability of highly diffusible substances by this technique and show that neither water nor the alcohols studied freely equilibrate with brain when the cerebral blood flow exceeds 30 ml/100 g min-1. At a cerebral blood flow of 50 ml/100 g min-1 only about 93% of an injected bolus of labeled water freely exchanges with brain, compared with methanol (93%), ethanol (97%), and isopropanol (99%). The brain capillary permeability-surface area (PS) products computed from these data were 0.023 cm3/s g-1 (water), 0.024 cm3/s g-1 (methanol), 0.030 cm3/s g-1 (ethanol), and 0.062 cm3/s g-1 (isopropanol). This sequence of PS products is consistent with the individual lipid solubilities of the alcohols studied and underscores the unique brain permeability characteristics of lipid-insoluble water.

Regional distribution of cerebral blood flow during exercise in dogs

1980 ◽  
Vol 48 (2) ◽  
pp. 213-217 ◽  
Author(s):  
P. M. Gross ◽  
M. L. Marcus ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Distribution ◽  
Moderate Intensity ◽  
Regional Cerebral Blood ◽  
Arterial Pco2 ◽  
Regional Flow ◽  
Arterial Blood ◽  
The Brain ◽  
Cerebral Vascular Resistance

This study was performed to determine whether exercise produces vasodilatation in regions of the brain that are associated with motor functions despite the associated vasoconstrictor effect of hypocapnia. Total and regional cerebral blood flow (CBF) were measured with microspheres in dogs during treadmill exercise of moderate intensity. Flow was also measured at rest after stimulation of ventilation with doxapram. During moderate exercise, total CBF was not changed significantly, but regional flow was increased in structures associated with motor-sensory control; blood flow to motor-sensory cortex, neocerebellar and paleocerebellar cortex, and spinal cord increased 30 +/- 7%, 39 +/- 8%, and 29 +/- 4%, respectively (P less than 0.05). After doxapram, which increased arterial blood pressure and decreased arterial PCO2 to levels similar to those during exercise, total CBF decreased and there was no redistribution of CBF. These results indicate that exercise in conscious dogs increases blood flow in regions of the brain associated with movement despite the associated vasoconstrictor stimulus of arterial hypocapnia. Thus, during exercise, local dilator influences that presumably result from increases in metabolism predominate over a potent constrictor stimulus in regulation of cerebral vascular resistance.

scholarly journals Time Course of Anoxia-Induced Increase in Cerebral Blood Flow Rate in Turtles: Evidence for a Role of Adenosine

1994 ◽  
Vol 14 (5) ◽  
pp. 877-881 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Rate ◽  
Time Course ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Systemic Blood Pressure ◽  
The Brain ◽  
Survival Mechanisms

The exceptional ability of the turtle brain to survive prolonged anoxia makes it a unique model for studying anoxic survival mechanisms. We have used epiillumination microscopy to record blood flow rate in venules on the cortical surface of turtles ( Trachemys scripta). During anoxia, blood flow rate increased 1.7 times after 45–75 min, whereupon it fell back, reaching preanoxic values after 115 min of anoxia. Topical super-fusion with adenosine (50 μ M) during normoxia caused a 3.8-fold increase in flow rate. Superfusing the brain with the adenosine receptor blocker aminophylline (250 μ M) totally inhibited the effects of both adenosine and anoxia, while aminophylline had no effect on normoxic flow rate. None of the treatments affected systemic blood pressure. These results indicate an initial adenosine-mediated increase in cerebral blood flow rate during anoxia, probably representing an emergency response before deep metabolic depression sets in.

scholarly journals Inhibition of Neuronal Nitric Oxide Synthase by 7-Nitroindazole: Effects upon Local Cerebral Blood Flow and Glucose Use in the Rat

1995 ◽  
Vol 15 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Paul A. T. Kelly ◽  
Isobel M. Ritchie ◽  
Gordon W. Arbuthnott
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Physiological Role ◽  
Neuronal Nitric Oxide Synthase ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Oxide Synthase ◽  
The Brain

The novel nitric oxide synthase inhibitor 7-nitroindazole (7-NI) is relatively specific for the neuronal isoform of the enzyme and in this study we have used this compound to investigate the physiological role of perivascular nitric oxide-containing nerves in the cerebrovascular bed. Following injection of 7-NI (25 or 50 mg/kg, i.p.), cerebral blood flow and glucose utilization were measured in the conscious rat using the fully quantitative [14C]iodoantipyrine and 2-[14C]deoxyglucose techniques, respectively. Neither dose of the drug produced any change in arterial blood pressure, confirming a lack of effect upon the endothelial isoform of the enzyme, although there was a pronounced decrease in heart rate (−28% by 10 min postinjection). Throughout the brain 25 mg/kg 7-NI i.p. resulted in decreases in blood flow of between −20% in the hippocampus and −58% in the substantia nigra. Increasing the dose to 50 mg/kg resulted in a further generalized decrease, to almost −60% in parts of the thalamus and hippocampus, but in every animal this higher dose of 7-NI also produced randomly distributed areas of relative hyperaemia, which were most commonly found in those areas where the most intense hypoperfusion was otherwise in evidence. Despite these changes in blood flow, in all but a very few areas of the brain no significant decrease in glucose use was measured at either of the two doses of 7-NI. Thus despite the greater specificity of 7-NI for neuronal nitric oxide synthase, the cerebrovascular effects of the drug in vivo are very similar to that reported for the arginine analogues. However, these data do suggest that nitric oxide-releasing neurones in the brain may have an important role to play in the regulation of cerebral blood flow.

scholarly journals Respiratory and circulatory control during sleep.

1982 ◽  
Vol 100 (1) ◽  
pp. 223-244
Author(s):  
J H Coote
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Partial Pressure ◽  
Arterial Blood ◽  
Circulatory Control ◽  
Differential Pattern ◽  
Vascular Beds ◽  
The Brain

A survey of the literature on a large number of vertebrate animals shows that sleep is associated with profound cardiovascular and respiratory adjustments which are very similar in each species. A hypothesis is advanced that these adjustments are 'goal directed' by neural structures in the brainstem, to ensure an adequate O2 and CO2 transport to and from the brain whilst at the same time reducing energy cost. During synchronised sleep there is a vagal bradycardia leading to reduced cardiac output and a fall in blood pressure; despite this cerebral blood flow increases. During desynchronized sleep there is a tonic fall in blood pressure and heart rate resulting from a unique repatterning of sympathetic discharge, that to heart, kidney, splanchnic and pelvic vascular beds decreasing whilst that to skeletal muscle increasing; cerebral blood flow shows a further increase. This differential pattern is probably initiated by neurones located in the caudal raphe nucleus obscurus. Phasic increases in blood pressure and heart rate also occur during desynchronized sleep mainly as a consequence of increases in sympathetic activity. Ventilation decreases during synchronized sleep accompanied by an increase in partial pressure of arterial CO2, which vasodilates cerebral blood vessels, indicating that the influence of CO2 on the level of ventilation has changed. During desynchronized sleep ventilation increases and becomes very irregular but the partial pressure of O2 and CO2 in arterial blood is little changed from wakefulness. Control of respiration is shifted to a central generator which apparently is different to the automatic/metabolic one which is normally dominant during wakefulness. Reflex control of the circulation and respiration is mainly governed by peripheral chemoreceptors, the threshold of most other afferent inputs being significantly raised during sleep.

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