scholarly journals Regional Changes in Cerebral Blood Flow and Blood — Brain Barrier Permeability during Epileptiform Seizures and in Acute Hypertension in Rabbits

1984 ◽  
Vol 4 (1) ◽  
pp. 96-102 ◽  
Author(s):  
R. Suzuki ◽  
C. Nitsch ◽  
K. Fujiwara ◽  
I. Klatzo
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Brain Barrier ◽  
Systemic Hypertension ◽  
Acute Hypertension ◽  
Arterial Blood ◽  
Blood Brain

Interrelationship between the breakdown of the blood–brain barrier (BBB) to Evans blue and elevations in the regional cerebral blood flow (rCBF) was studied in rabbits subjected to adrenaline- or metaraminol-induced systemic hypertension and also in bicuculline-induced seizures. The rCBF was assessed in small samples from various regions of the brain with the use of [3H]nicotine, and the permeability of the BBB was evaluated with an Evans blue tracer. In acute hypertension, Evans blue extravasations were observed in the occipital cortex and sometimes in the superior colliculus, i.e., the regions which also showed the highest elevations in rCBF. The breakdown of the BBB in acute hypertension was clearly related to the rate of mean arterial blood pressure rise, being much less pronounced in the metaraminol group, which showed a much slower blood pressure elevation rate. In bicuculline-induced seizures, there was no evident correlation between the amplitude of rCBF elevations and Evans blue extravasations. Preservation of BBB integrity was observed in areas showing high elevations in the rCBF.

scholarly journals Effect of the Calcium Antagonist, Nimodipine, on Cerebral Blood Flow and Metabolism in the Primate

1981 ◽  
Vol 1 (3) ◽  
pp. 349-356 ◽  
Author(s):  
A. M. Harper ◽  
L. Craigen ◽  
S. Kazda
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Calcium Antagonist ◽  
Arterial Blood Pressure ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Arterial Blood ◽  
Blood Brain ◽  
Significant Change

The effect of the calcium antagonist nimodipine was tested in anaesthetised primates. A rapid intravenous injection of 3 or 10 μg kg−1 produced a transient rise in end-tidal Pco2 and a fall in arterial blood pressure, but 10 min after the injection there was no significant change in CBF. A continuous intravenous infusion of 2 μg kg−1 min−1 caused a modest fall in mean arterial blood pressure and an increase in cerebral blood flow (CBF), which gradually increased to 27% above control after 50 min infusion. There was no significant change in CMRO2. A continuous intracarotid infusion of 0.67 μg kg−1 min−1 caused an increase in CBF of between 46 and 57%. This was further increased to 87% above control after disruption of the blood-brain barrier with hyperosmolar urea. Thirty minutes after the urea, the CBF returned to 43% above control. Twenty minutes after the infusion of nimodipine had been stopped, the CBF had returned to control values. EEG studies in this group showed no obvious increase in electrocortical activity. This evidence suggests that nimodipine has no effect on cerebral metabolism but increases CBF, particularly after disruption of the blood-brain barrier.

The influence of nimodipine on cerebral blood flow autoregulation and blood-brain barrier

1988 ◽  
Vol 69 (6) ◽  
pp. 919-922 ◽  
Author(s):  
Hans-Georg Höllerhage ◽  
Michael R. Gaab ◽  
Matthias Zumkeller ◽  
Gerhard F. Walter
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Brain Barrier ◽  
Control Group ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Blood Brain ◽  
Anesthetized Rats

✓ Twenty anesthetized rats were randomly assigned to a nimodipine-treated group or a control group of 10 rats each. Local cerebral blood flow (lCBF) was measured by means of a surface electrode using the hydrogen clearance technique. Systemic arterial pressure (SAP) was varied with administration of norfenefrine or by hemorrhage in order to obtain SAP/cerebral blood flow (CBF) curves under different conditions. In the control group, a typical autoregulation curve was obtained with an lCBF plateau between 70 and 120 mm Hg SAP. The nimodipine-treated animals, however, showed only a slight diminution in the slope of the curve but no real plateau, indicating impairment of CBF autoregulation. In another series, 20 anesthetized rats were randomly assigned to a treatment group or a control group of 10 animals each. Intravenous Evans blue dye was used as a tracer for blood-brain barrier (BBB) function. In both groups, SAP was raised to a level of 180 mm Hg with administration of norfenefrine for 6 minutes. Extravasation of significantly more Evans blue dye was observed in the nimodipine group than in the control group, indicating impairment of the BBB. It is concluded that nimodipine may impair CBF autoregulation, allowing damage to the BBB under hypertensive conditions.

Time courses of changes in cerebral blood flow and blood-brain barrier integrity by focal proton radiation in the rat

1996 ◽  
Vol 18 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Hiroki Namba ◽  
Toshiaki Irie ◽  
Kiyoshi Fukushi ◽  
Masaomi lyo ◽  
Takahiro Hashimoto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Proton Radiation ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Time Courses ◽  
Blood Brain Barrier Integrity

Effect of sympathetic nerves on cerebral vessels during seizures

1979 ◽  
Vol 237 (2) ◽  
pp. H178-H184 ◽  
Author(s):  
S. M. Mueller ◽  
D. D. Heistad ◽  
M. L. Marcus
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Nerves ◽  
Brain Barrier ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Cervical Sympathetic ◽  
The Brain

The purpose of this study was to determine the effect of activation of sympathetic pathways during seizures on cerebral blood flow and integrity of the blood-brain barrier. We measured cerebral blood flow with microspheres and disruption of the blood-brain barrier with labeled albumin in cats. One cerebral hemisphere was denervated by cutting the superior cervical sympathetic trunk on one side. During bicuculline-induced seizures, superior cervical sympathetic nerve activity increased about threefold. Blood flow to the innervated hemibrain was significantly lower than flow to denervated hemibrain. However, in relation to the total increase in flow, this effect of nerves was minor. Blood-brain barrier permeability increased about sixfold during seizures, but there was no difference between the innervated and denervated sides of the brain. We conclude that sympathetic nerves attenuate the increase in cerebral blood flow during seizures, despite the increase in metabolism, but this effect is small. Activation of sympathetic nerves does not reduce disruption of the blood-brain barrier during seizures.

scholarly journals Blood—Brain Barrier Transport of Butanol and Water Relative to N-Isopropyl-p-Iodoamphetamine as the Internal Reference

1985 ◽  
Vol 5 (2) ◽  
pp. 275-281 ◽  
Author(s):  
William M. Pardridge ◽  
Gary Fierer
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Internal Reference ◽  
Diffusion Restriction ◽  
Blood Brain ◽  
Anesthetized Rats ◽  
Rat Forebrain ◽  
The Brain

The literature regarding the blood–brain barrier (BBB) transport of butanol is conflicting as studies report both incomplete and complete extraction of butanol by the brain. In this work the BBB transport of both [14C]butanol and [3H]water was studied using the carotid injection technique in conscious and in ketamine- or pentobarbital-anesthetized rats employing N-isopropyl- p-[125I]iodoamphetamine ([125I]IMP) as the internal reference and as a fluid microsphere. The three isotopes (3H, 125I, 14C) were conveniently counted simultaneously in a liquid scintillation spectrometer. IMP is essentially completely sequestered by the brain for at least 1 min in conscious rats and for 2 min in anesthetized animals. Butanol extraction by rat forebrain is not flow limited but ranges between 77 ± 1 and 87 ± 1% for the three conditions. The incomplete extraction of butanol by the forebrain is due to diffusion restriction of butanol clearance in some regions (frontal cortex, colliculi) but not in others (caudate, hippocampus, olfactory bulb). The permeability-surface area product/cerebral blood flow ratio of butanol and water in rat forebrain remains relatively constant, 1.7 ± 0.2 and 1.0 ± 0.1, respectively, despite a twofold increase in cerebral blood flow in conscious relative to pentobarbital-anesthetized rats. The absence of an inverse relationship between flow and butanol or water extraction is consistent with capillary recruitment being the principal mechanism underlying changes in cerebral blood flow in anesthesia. The diffusion restriction of BBB transport of butanol in some regions, but not in others, necessitates a careful regional analysis of BBB permeability to butanol prior to usage of this compound as a cerebral blood flow marker.

scholarly journals Dynamic in vivo imaging of cerebral blood flow and blood–brain barrier permeability

NeuroImage ◽  
2010 ◽  
Vol 49 (1) ◽  
pp. 337-344 ◽  
Author(s):  
Ofer Prager ◽  
Yoash Chassidim ◽  
Chen Klein ◽  
Haviv Levi ◽  
Ilan Shelef ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
In Vivo Imaging ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability
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