Cerebrospinal fluid may nourish cerebral vessels through pathways in the adventitia that may be analogous to systemic vasa vasorum

Zervas, Nicholas T.; Liszczak, Theodore M.; Mayberg, Marc R.; Black, Peter McL.

doi:10.3171/jns.1982.56.4.0475

Cited by 156 publications

(58 citation statements)

References 2 publications

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“…Potential routes of entry from the CSF into the PVS include specialized pores, termed stomata, recently demonstrated on the adventitial lining cells of leptomeningeal vessels in the SAS of the rat by scanning electron microscopy [137] (Fig. 1b), confirming earlier decades-old identification of such structures in cats [199]; similar pores may also exist on the pia [30,146], providing an additional route into the PVS via the subpial space (discussed in [137]). It has become increasingly clear that substances within the CSF may potentially access and distribute along the PVS to varying extents all throughout the cerebrovascular tree, e.g., large full length antibodies (immunoglobulin G) have been shown to access the PVS of arterioles (Fig.…”

Section: Blood Vessels and The Perivascular Spacesupporting

confidence: 55%

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

et al. 2018

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Brain fluids are rigidly regulated to provide stable environments for neuronal function, e.g., low K + , Ca 2+ , and protein to optimise signalling and minimise neurotoxicity. At the same time, neuronal and astroglial waste must be promptly removed. The interstitial fluid (ISF) of the brain tissue and the cerebrospinal fluid (CSF) bathing the CNS are integral to this homeostasis and the idea of a glia-lymph or 'glymphatic' system for waste clearance from brain has developed over the last 5 years. This links bulk (convective) flow of CSF into brain along the outside of penetrating arteries, glia-mediated convective transport of fluid and solutes through the brain extracellular space (ECS) involving the aquaporin-4 (AQP4) water channel, and finally delivery of fluid to venules for clearance along peri-venous spaces. However, recent evidence favours important amendments to the 'glymphatic' hypothesis, particularly concerning the role of glia and transfer of solutes within the ECS. This review discusses studies which question the role of AQP4 in ISF flow and the lack of evidence for its ability to transport solutes; summarizes attributes of brain ECS that strongly favour the diffusion of small and large molecules without ISF flow; discusses work on hydraulic conductivity and the nature of the extracellular matrix which may impede fluid movement; and reconsiders the roles of the perivascular space (PVS) in CSF-ISF exchange and drainage. We also consider the extent to which CSF-ISF exchange is possible and desirable, the impact of neuropathology on fluid drainage, and why using CSF as a proxy measure of brain components or drug delivery is problematic. We propose that new work and key historical studies both support the concept of a perivascular fluid system, whereby CSF enters the brain via PVS convective flow or dispersion along larger caliber arteries/arterioles, diffusion predominantly regulates CSF/ISF exchange at the level of the neurovascular unit associated with CNS microvessels, and, finally, a mixture of CSF/ISF/waste products is normally cleared along the PVS of venules/veins as well as other pathways; such a system may or may not constitute a true 'circulation', but, at the least, suggests a comprehensive re-evaluation of the previously proposed 'glymphatic' concepts in favour of a new system better taking into account basic cerebrovascular physiology and fluid transport considerations.

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Section: Blood Vessels and The Perivascular Spacesupporting

confidence: 55%

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

et al. 2018

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“…It has been reported that injection of leucine into the cisterna magna in cats resulted in a subtle accumulation of the amino acid within 1 min in the entire extracellular space, including that of the intima, of the cerebral vessel wall (Zervas, Liszczak, Mayberg & Black, 1982). Also, in the present study, in which vasopressin was applied directly to the adventitial surface for a period of at least 3 min, the vasopressin might have gained access to the endothelium.…”

Section: Discussionmentioning

confidence: 67%

Contractile effects of perivascularly applied vasopressin on the pial artery of the cat brain.

Nakai

1987

The Journal of Physiology

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SUMMARY1. The effects of perivascularly applied vasopressin on the diameter of pial arteries (control 298 + 14 S.E. ,m) of the brain were examined after chronic implantation of a cranial window in fifteen anaesthetized cats.2. Application of vasopressin resulted in a dose-dependent contraction. The threshold concentration for contraction was 3 x 10-10 M, the half-maximal effective concentration (ED50) (16±+02) x 10-9 M, and the maximum reduction in artery diameter 37 + 2 /.3. The contraction was powerfully inhibited by perivascular application of a 10-M solution of the vasopressin antagonist, [1-(,8-mercapto-,8,,8-cyclopenta-methylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin. 4. Perivascular application ofnoradrenaline induced a dose-dependent contraction of the pial artery. The ED50 was (8-9 + 2 5) x 10-7 M, and the maximum reduction in artery diameter was 33 + 2 %.5. Such noradrenaline-induced contraction was not modified at all in the presence of a subthreshold dose (2 x 10-10 M) of vasopressin (P > 0 05, for the over-all difference in size of the contraction, ED50 and maximum contraction).6. In another experimental setting it was also found that neither the subthreshold nor a suprathreshold (10-9 M) dose of vasopressin modified the contraction induced by 10-6 M-noradrenaline (P > 0 05, compared to the contraction in the absence of vasopressin).7. Thus a powerful and sensitive contractile response of the pial arteries to perivascularly applied vasopressin was demonstrated. However, the modifying effect of vasopressin on the contraction induced by perivascularly applied noradrenaline was minimal.

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“…33 This is possible because the surfaces of the pial cerebral arteries are, exceptionally, not confined by collagen or fibroblasts but are in direct contact with the nourishing CSF. 33 Indeed, it has been shown that ET-1 acts from the adventitial but not the luminal side of the vessel. 34 This is consistent with our observation of a release of ET-1 by leukocytes in the subarachnoid space.…”

Section: Faßbender Et Al Et-1 In Subarachnoid Hemorrhage 2973mentioning

confidence: 99%

Endothelin-1 in Subarachnoid Hemorrhage

Faßbender

Hodapp

Rossol

et al. 2000

Stroke

142

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Background and Purpose-The most potent vasoconstrictor known, endothelin-1, is currently considered to mediate cerebral vasospasm in subarachnoid hemorrhage (SAH), which can cause delayed cerebral ischemia. In our study, we performed clinical and in vitro experiments to investigate the origin and the mechanisms of the secretion of endothelin-1 in SAH. Methods-Endothelin-1 and markers of inflammatory host response (interleukin [IL]-1␤, IL-6, and tumor necrosis factor-␣) were comparatively quantified in the cerebrospinal fluid (CSF) of SAH patients and control subjects, and concentrations were related to clinical characteristics. Furthermore, mononuclear leukocytes isolated from the CSF of SAH patients and control subjects were analyzed regarding their mRNA expression of endothelin-1 and inflammatory cytokines. Finally, complementary in vitro experiments were performed to investigate whether coincubation of blood and CSF can trigger leukocytic mRNA expression and release of these factors. Results-Activated mononuclear leukocytes in the CSF of SAH patients synthesize and release endothelin-1 in parallel with known acute-phase reactants (IL-1␤, IL-6, and tumor necrosis factor-␣). Complementary in vitro experiments not only further confirmed this leukocytic origin of endothelin-1 but also showed that aging and subsequent hemolysis of blood is sufficient to induce such endothelin-1 production. Conclusions-The demonstration that endothelin-1 is produced by activated CSF mononuclear leukocytes suggests that subarachnoid inflammation may represent a therapeutic target to prevent vasospasm and delayed cerebral ischemia after SAH. (Stroke. 2000;31:2971-2975.)

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Cerebrospinal fluid may nourish cerebral vessels through pathways in the adventitia that may be analogous to systemic vasa vasorum

Cited by 156 publications

References 2 publications

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?

Contractile effects of perivascularly applied vasopressin on the pial artery of the cat brain.

Endothelin-1 in Subarachnoid Hemorrhage

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