scholarly journals Cerebral Blood Flow in Cats After an Acute Hypertensive Insult With Damage to the Blood-Brain Barrier

Stroke ◽  
1975 ◽  
Vol 6 (2) ◽  
pp. 188-198 ◽  
Author(s):  
J. L. PANNIER ◽  
I. LEUSEN
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

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

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.

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

scholarly journals Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model

1996 ◽  
Vol 1 (4) ◽  
pp. E3 ◽  
Author(s):  
Kevin R. Lee ◽  
Nobuyuki Kawai ◽  
Seoung Kim ◽  
Oren Sagher ◽  
Julian T. Hoff
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracerebral Hemorrhage ◽  
Blood Brain Barrier ◽  
Brain Slices ◽  
Brain Barrier ◽  
C6 Glioma Cells ◽  
Edema Formation ◽  
Blood Brain

Recently, the authors showed that thrombin contributes to the formation of brain edema following intracerebral hemorrhage. The current study examines whether the action of thrombin is due to an effect on cerebral blood flow (CBF), vasoreactivity, blood-brain barrier (BBB) function, or cell viability. In vivo solutions of thrombin were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; CBF and BBB permeability were measured. The actions of thrombin on vasoreactivity were examined in vitro by superfusing thrombin on cortical brain slices while monitoring microvessel diameter with videomicroscopy. In separate experiments C6 glioma cells were exposed to various concentrations of thrombin and lactate dehydrogenase release, a marker of cell death, was measured. The results indicate that thrombin induces BBB disruption as well as death of parenchymal cells, whereas CBF and vasoreactivity are not altered. The authors conclude that cell toxicity and BBB disruption by thrombin are triggering mechanisms for the edema formation that follows intracerebral hemorrhage.

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