Cerebral Vascular Permeability Research Articles

The Blood-Retinal Barriers

This text contains material from a series of lectures by distinguished scientists and clinicians who participated in the Advanced Study Institutes series on blood-retinal barriers that was held in Espinho, Portugal, in September 1979. The book is divided into the following parts: general aspects of membrane permeability; sites and functions of the blood-brain and blood-retinal barriers; transport at the blood-brain and blood-retinal barriers; methods of evaluation of the blood-retinal barriers, including vitreous fluorophotometry and fluorescein angiography; pathologic characteristics of the blood-retinal barriers; and clinical importance of alterations of the blood-retinal barriers. Ophthalmologists will find the first half of this book highly technical. The authors deal with current concepts having to do with the structure and function of cell membranes; the biophysical aspects of membrane permeability; the relationship of cerebral endothelium and astrocytic membranes; cerebral vascular permeability after osmotic changes; sites and functions of blood-retinal barriers, as well as alterations of

Cerebral microvessels contain A β2-adrenergic receptor

Cerebral microvessels isolated from cat forebrain contain a specific β-adrenergic-sensitive adenylate cyclase. Among various compounds tested, the most potent activator of enzyme activity is isoproterenol (k a = 1.4 × 10 −7M), followed in order by epinephrine (k a= 1.5 × 10 −6M), norepinephrine (k a= 1.4 × 10 −5M) and phenylephrine (k a> 3 × 10 −4M). Isoproterenol-stimulated enzyme activity is blocked by propranolol (k i= 2.4 × 10 −9M, IPS 339 (k i= 4 × 10 −9M), H35/25 (k i = 1.2 × 10 −7M), atenolol (k i= 5.9 × 10 −6M) and practolol (k i= 1.8 × 10 −5M). These agonist and antagonist properties are quite similar to those demonstrated by β 2-adrenergic receptors and β 2-stimulated adenylate cyclase present in other tissues and indicate that the majority of adenylate cyclase-associated adrenergic receptors in cerebral microvessels are β 2. The findings are relevant to physiological studies of cerebral blood flow and vascular permeability.

Identification of β-adrenergic-sensitive adenylate cyclase in intracranial blood vessels

THE regulation of cerebral blood flow and vascular permeability is important in such clinical conditions as stroke, arterial spasm, vascular headache (for example, migraine) and metabolic effects of seizures. Unfortunately, relatively little is known about the nervous control of cerebral circulation, particularly with regard to the nature of the hormone and neurotransmitter receptors present in cerebral vessels. An influence of the adrenergic nervous system has been suggested by histological studies showing that the blood vessels and branches of the circle of Willis receive innervation from the sympathetic chain1, and that the smaller, penetrating cerebral vessels (called microvessels) are surrounded by noradrenaline-containing fibres which seem to arise from brainstem nor adrenergic nuclei2,3. Although attempts to demonstrate β-adrenergic receptors in cerebral vascular tissue by cytochemical methods have been unsuccessful4, indirect evidence for the presence of such receptors is suggested by reports that adrenergic stimulation can alter cerebral blood flow and vascular permeability3,5, and that cate-cholamine agonists (such as isoprenaline and adrenaline) can dilate whole-artery preparations of cerebral vessels6. We now report the presence of a β-adrenergic-stimulated adenylate cyclase in both superficial and deep cerebral blood vessels. In addition to supplying direct biochemical evidence for the existence of β-adrenergic receptors in the cerebral vasculature, identification of this enzyme should facilitate the evaluation of the actions of pharmacological agents on cerebral blood flow and vascular permeability.

The effect of hypercapnia on a blood-brain barrier mechanism in foetal and new-born sheep.

1. The effect of marked hypercapnia (arterial PCO2 100 mmHg), nonrespiratory acidosis (pH 6-95-7-15) or hypoxia (arterial PO2 10-15 mmHg) upon penetration of labelled sucrose from blood into brain and c.s.f. has been investigated in exteriorized foetal sheep and new-born lambs. 2. In hypercapnia there was a consistent increase in c.s.f./plasma sucrose ratio after 90 min I.V. sucrose to four to five times control. Brain/plasma sucrose ratios were more variable. Usually there was an increase (up to three-and-a-half-times control); sometimes there was no change or even a decrease. The effect of hypercapnia on sucrose penetration was reversible. 3. Hypercapnia reduced c.s.f. secretion rate to approximately half the control value. Hypercapnia also caused a decrease in brain extracellular space. 4. Non-respiratory acidosis did not affect sucrose penetration. Hypoxia caused a decrease in brain/plasma sucrose ratio. 5. It is concluded that hypercapnia can cuase an increase in cerebral vascular permeability to sucrose in foetal and new-born sheep. Some possible mechanisms are discussed.

Central noradrenergic regulation of cerebral blood flow and vascular permeability.

Anatomical studies employing the immunofluorescence localization of dopamine-beta-hydroxylase [= dopamine beta-monooxygenase; 3,4-dihydroxyphenylethylamine, ascorbate:oxygen oxidoreductase (beta-hydroxylating); EC 1.14.17.1] have demonstrated in brain central noradrenergic nerve fibers on small intraparenchymal blood vessels, including capillaries. This system is distinct from the peripheral noradrenergic system inervating the large extraparenchymal blood vessels. From these anatomical findings evolved the working hypothesis that the central noradrenergic system is analogous to the peripheral sympathetic system except that it is specialized for performing specific functions related to the brain microvasculature. To test this hypothesis cerebral blood flow and the brain vascular permeability of water (H215O) were measured in four adult rhesus monkeys (three with bilateral superior cervical ganglionectomies) with stereotaxically placed cannulae permanently located in the lateral ventricles and the locus coeruleus for the injection of drugs. Our data demonstrate that stimulation of the noradrenergic cell bodies in the locus coeruleus with carbachol (8 mug) produces a prompt reduction in hemispheric cerebral blood flow and an increase in brain vascular permeability of water. The intraventricular administration of the alpha-adrenergic blocker phentolamine (25--50 mug) has the opposite effect. These preliminary data support the hypothesis that the central noradrenergic system is analogous to the peripheral sympathetic system with the special function of regulating brain vascular permeability as well as blood flow.

Effect of increased intravascular pressure on the blood-brain barrier to protein in dogs.

In a previous study it was suggested that the cerebral vascular permeability dysfunction occurring in acute arterial hypertension was caused by the increased intraluminal pressure. The aim of the present experiments was to study further this effect on the blood-brain barrier. To rule out any ischemic influence cerebral vasodilatation was brought about by papaverine injection or CO2 inhalation and the cerebral blood flow measured and shown to be above normal before the blood pressure rise was induced. A sudden elevation of the systemic blood pressure still resulted in increased cerebral permeability indicated by Evans Blue extravasation. In one dog it was shown that an extremely rapid intracarotid autotransfusion resulted in a marked increase in the cerebral venous pressure and small areas of Evans Blue extravasation. Our results support the hypothesis that the permeability changes were caused by the increased intraluminal pressure.

The influence of carbon dioxide inhalation on the cerebral vascular permeability to trypan blue (the blood-brain barrier).

The influence of carbon dioxide inhalation on the cerebral vascular permeability to trypan blue (the blood-brain barrier).

SUPRAVITAL ANALYSIS OF DISORDERS IN THE CEREBRAL VASCULAR PERMEABILITY II. TWO CASES OF MULTIPLE SCLEROSIS

Acta Psychiatrica ScandinavicaVolume 22, Issue S46 p. 58-71 SUPRAVITAL ANALYSIS OF DISORDERS IN THE CEREBRAL VASCULAR PERMEABILITY II. TWO CASES OF MULTIPLE SCLEROSIS TORE BROMAN, TORE BROMAN LUNDSearch for more papers by this author TORE BROMAN, TORE BROMAN LUNDSearch for more papers by this author First published: October 1947 https://doi.org/10.1111/j.1600-0447.1947.tb08101.xCitations: 25AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume22, IssueS46October 1947Pages 58-71 RelatedInformation