Heterogeneity of brain blood flow and permeability during acute hypertension

1985 ◽  
Vol 249 (3) ◽  
pp. H629-H637 ◽  
Author(s):  
G. L. Baumbach ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Blood Brain Barrier ◽  
Regional Differences ◽  
Severe Hypertension ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
The Brain ◽  
Increased Blood Flow

The purpose of this study was to examine regional autoregulation of blood flow in the brain during acute hypertension. In anesthetized cats severe hypertension increased blood flow more in cerebrum (159%) and cerebellum (106%) than brain stem (58%). In contrast to the heterogeneous autoregulatory response, hypocapnia produced uniform vasoconstriction in the brain. We also compared vasodilatation during severe hypertension with vasodilatation during hypercapnia. During hypercapnia, blood flow increased as much in brain stem, as in cerebrum and cerebellum. Thus regional differences in autoregulation appear to be specific for autoregulatory stimulus and are not secondary to nonspecific differences in vasoconstrictor or vasodilator capacity. To determine whether the blood-brain barrier is more susceptible to hypertensive disruption in regions with less effective autoregulation, permeability of the barrier was quantitated with 125I-albumin. Severe hypertension produced disruption of the barrier in cerebrum but not in brain stem. Thus there are parallel differences in effectiveness of autoregulation and susceptibility to disruption of the blood-brain barrier in different regions of the brain.

Disruption of the blood-brain barrier in cerebrum and brain stem during acute hypertension

1986 ◽  
Vol 251 (6) ◽  
pp. H1171-H1175 ◽  
Author(s):  
W. G. Mayhan ◽  
F. M. Faraci ◽  
D. D. Heistad
Keyword(s):  
Arterial Pressure ◽  
Brain Stem ◽  
Blood Brain Barrier ◽  
Venous Pressure ◽  
Fluorescent Microscopy ◽  
Systemic Arterial Pressure ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
The Brain

The purpose of this study was to examine hemodynamic mechanisms of protection of the blood-brain barrier in the brain stem during acute hypertension. We used a new method to examine the microcirculation of the brain stem. Intravital fluorescent microscopy and fluorescein-labeled dextran were used to evaluate disruption of the blood-brain barrier during acute hypertension in rats. During control conditions, pressure (servo null) in arterioles (60 microns in diameter) was 50 +/- 2% (mean +/- SE) of systemic arterial pressure in the cerebrum and 67 +/- 1% of systemic arterial pressure in the brain stem (P less than 0.05 vs. cerebrum). In the cerebrum, pial venous pressure increased from 7 +/- 1 to 25 +/- 2 mmHg during acute hypertension, and there was marked disruption of the blood-brain barrier in venules (26 +/- 2 leaky sites). In contrast, in the brain stem, pial venous pressure increased from 4 +/- 1 to only 8 +/- 1 mmHg (P less than 0.05 vs. cerebrum), and there was minimal disruption of the blood-brain barrier in venules (1.5 +/- 0.6 leaky sites, P less than 0.05 vs. cerebrum). During acute hypertension, increases in blood flow (microspheres) were less in brain stem than in cerebrum. The findings suggest distribution of vascular resistance differs in the brain stem and cerebrum under control conditions, whereas large arteries account for a greater fraction of resistance in cerebrum; pial venous pressure increases less in brain stem than cerebrum during acute hypertension, so that the blood-brain barrier is protected.(ABSTRACT TRUNCATED AT 250 WORDS)

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 Effects of sympathetic nerves on cerebral vessels in dog, cat, and monkey

1978 ◽  
Vol 235 (5) ◽  
pp. H544-H552 ◽  
Author(s):  
D. D. Heistad ◽  
M. L. Marcus ◽  
P. M. Gross
Keyword(s):  
Blood Brain Barrier ◽  
Severe Hypertension ◽  
Species Difference ◽  
Cerebral Vessels ◽  
Brain Barrier ◽  
Sympathetic Stimulation ◽  
Acute Hypertension ◽  
Important Species ◽  
Blood Brain ◽  
Cervical Sympathetic

Cerebral vascular responses to sympathetic stimulation and denervation were examined in three species during acute severe hypertension as well as normal conditions. Cerebral blood flow (CBF) was measured with microspheres after the superior cervical sympathetic trunk was cut and during electrical stimulation of the superior cervical sympathetic ganglion. Sympathetic denervation did not increase CBF in anesthetized cats or monkeys. Under normal conditions, sympathetic stimulation decreased CBF significantly in monkeys (-26 +/- 3%) (mean +/- SE) but not in cats. During acute severe hypertension, decreases in CBF due to sympathetic stimulation were greatly augmented in cats (-29 +/- 7%, compared to -3 +/- 3%), only modestly augmented in dogs (-9 +/- 3%, compared to -1 +/- 2%), and not augmented in monkeys (-17 +/- 3%, compared to -23 +/- 4%). Disruption of the blood-brain barrier during hypertension was reduced by sympathetic stimulation. We conclude that 1) sympathetic tone to cerebral vessels is minimal because denervation does not increase CBF; 2) sympathetic stimulation decreases CBF under normal conditions in monkeys and during severe hypertension in cats, dogs, and monkeys, and it reduces disruption of the blood-brain barrier; and 3) there is an important species difference in responses to sympathetic stimulation under normal conditions and during acute hypertension.

scholarly journals Neurotropic Lineage III Strains of Listeria monocytogenes Disseminate to the Brain without Reaching High Titer in the Blood

mSphere ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
Taylor E. Senay ◽  
Jessica L. Ferrell ◽  
Filip G. Garrett ◽  
Taylor M. Albrecht ◽  
Jooyoung Cho ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Mouse Model ◽  
Brain Stem ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Neurological Deficits ◽  
Content Type ◽  
Phylogenetic Lineage ◽  
Blood Brain ◽  
The Brain

ABSTRACT Listeria monocytogenes is thought to colonize the brain using one of three mechanisms: direct invasion of the blood-brain barrier, transportation across the barrier by infected monocytes, and axonal migration to the brain stem. The first two pathways seem to occur following unrestricted bacterial growth in the blood and thus have been linked to immunocompromise. In contrast, cell-to-cell spread within nerves is thought to be mediated by a particular subset of neurotropic L. monocytogenes strains. In this study, we used a mouse model of foodborne transmission to evaluate the neurotropism of several L. monocytogenes isolates. Two strains preferentially colonized the brain stems of BALB/cByJ mice 5 days postinfection and were not detectable in blood at that time point. In contrast, infection with other strains resulted in robust systemic infection of the viscera but no dissemination to the brain. Both neurotropic strains (L2010-2198, a human rhombencephalitis isolate, and UKVDL9, a sheep brain isolate) typed as phylogenetic lineage III, the least characterized group of L. monocytogenes. Neither of these strains encodes InlF, an internalin-like protein that was recently shown to promote invasion of the blood-brain barrier. Acute neurologic deficits were observed in mice infected with the neurotropic strains, and milder symptoms persisted for up to 16 days in some animals. These results demonstrate that neurotropic L. monocytogenes strains are not restricted to any one particular lineage and suggest that the foodborne mouse model of listeriosis can be used to investigate the pathogenic mechanisms that allow L. monocytogenes to invade the brain stem. IMPORTANCE Progress in understanding the two naturally occurring central nervous system (CNS) manifestations of listeriosis (meningitis/meningoencephalitis and rhombencephalitis) has been limited by the lack of small animal models that can readily distinguish between these distinct infections. We report here that certain neurotropic strains of Listeria monocytogenes can spread to the brains of young otherwise healthy mice and cause neurological deficits without causing a fatal bacteremia. The novel strains described here fall within phylogenetic lineage III, a small collection of L. monocytogenes isolates that have not been well characterized to date. The animal model reported here mimics many features of human rhombencephalitis and will be useful for studying the mechanisms that allow L. monocytogenes to disseminate to the brain stem following natural foodborne transmission.

Effect of atriopeptin on blood flow to cerebrum and choroid plexus

1989 ◽  
Vol 257 (6) ◽  
pp. R1365-R1369
Author(s):  
K. A. Schalk ◽  
J. L. Williams ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Choroid Plexus ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Increased Blood Flow

The goal of this study was to determine whether atriopeptin alters blood flow to cerebrum and choroid plexus. In anesthetized rabbits, blood flow (microspheres) to cerebrum and choroid plexus under control conditions was 36 +/- 3 (mean +/- SE) and 573 +/- 78 ml.min-1.100 g-1, respectively. Infusion of atriopeptin (75, 225, 1,150 ng.kg-1.min-1 iv) increased blood flow to choroid plexus by 22 +/- 11, 53 +/- 26, and 51 +/- 13%, respectively. In contrast, blood flow to cerebrum was not altered by atriopeptin, presumably because the blood-brain barrier prevented access to cerebral vascular smooth muscle. Because a major role of atriopeptin may be to modulate responses to angiotensin II, we examined effects of atriopeptin on vasoconstrictor responses to angiotensin II in the choroid plexus. Angiotensin II was infused in the presence or absence of atriopeptin (300 ng.kg-1.min-1 iv). Angiotensin II (100 ng.kg-1.min-1 iv) decreased blood flow to choroid plexus by 49 +/- 12% and by 47 +/- 14% during simultaneous infusion of atriopeptin. In summary, atriopeptin 1) increases blood flow to choroid plexus, but not cerebrum, and 2) does not appear to attenuate vasoconstrictor effects of angiotensin II in the choroid plexus.

scholarly journals Neurobarrier Coupling in the Brain: A Partner of Neurovascular and Neurometabolic Coupling?

2005 ◽  
Vol 25 (1) ◽  
pp. 2-16 ◽  
Author(s):  
Luc Leybaert
Keyword(s):  
Blood Flow ◽  
Glucose Transport ◽  
Blood Brain Barrier ◽  
Neural Tissue ◽  
Brain Barrier ◽  
Neuronal Activation ◽  
Transport Parameters ◽  
Blood Brain ◽  
Neurometabolic Coupling ◽  
The Brain

Neurovascular and neurometabolic coupling help the brain to maintain an appropriate energy flow to the neural tissue under conditions of increased neuronal activity. Both coupling phenomena provide us, in addition, with two macroscopically measurable parameters, blood flow and intermediate metabolite fluxes, that are used to dynamically image the functioning brain. The main energy substrate for the brain is glucose, which is metabolized by glycolysis and oxidative breakdown in both astrocytes and neurons. Neuronal activation triggers increased glucose consumption and glucose demand, with new glucose being brought in by stimulated blood flow and glucose transport over the blood-brain barrier. Glucose is shuttled over the barrier by the GLUT-1 transporter, which, like all transporter proteins, has a ceiling above which no further stimulation of the transport is possible. Blood-brain barrier glucose transport is generally accepted as a nonrate-limiting step but to prevent it from becoming rate-limiting under conditions of neuronal activation, it might be necessary for the transport parameters to be adapted to the increased glucose demand. It is proposed that the blood-brain barrier glucose transport parameters are dynamically adapted to the increased glucose needs of the neural tissue after activation according to a neurobarrier coupling scheme. This review presents neurobarrier coupling within the current knowledge on neurovascular and neurometabolic coupling, and considers arguments and evidence in support of this hypothesis.

Protection of the blood-brain barrier by hypercapnia during acute hypertension

1986 ◽  
Vol 251 (2) ◽  
pp. H282-H287
Author(s):  
G. L. Baumbach ◽  
W. G. Mayhan ◽  
D. D. Heistad
Keyword(s):  
Blood Brain Barrier ◽  
Severe Hypertension ◽  
Venous Pressure ◽  
Sympathetic Nerves ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
Cerebral Vasodilatation ◽  
Fluorescent Dextran ◽  
Incremental Increase

The purpose of this study was to examine effects of hypercapnia on susceptibility of the blood-brain barrier to disruption during acute hypertension. Two methods were used to test the hypothesis that cerebral vasodilatation during hypercapnia increases disruption of the blood-brain barrier. First, permeability of the blood-brain barrier was measured in anesthetized cats with 125I-labeled serum albumin. Severe hypertension markedly increased permeability of the blood-brain barrier during normocapnia, but not during hypercapnia. The protective effect of hypercapnia was not dependent on sympathetic nerves. Second, in anesthetized rats, permeability of the barrier was quantitated by clearance of fluorescent dextran. Disruption of the blood-brain barrier during hypertension was decreased by hypercapnia. Because disruption of the blood-brain barrier occurred primarily in pial venules, we also measured pial venular diameter and pressure (with a servo-null method). Acute hypertension increased pial venular pressure and diameter in normocapnic rats. Hypercapnia alone increased pial venular pressure and pial venular diameter, and acute hypertension during hypercapnia further increased venular pressure. The magnitude of increase in pial venular pressure during acute hypertension was significantly less in hypercapnic than in normocapnic rats. We conclude that hypercapnia protects the blood-brain barrier. Possible mechanisms of this effect include attenuation of the incremental increase in pial venular pressure by hypercapnia or a direct effect on the blood-brain barrier not related to venous pressure.

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