scholarly journals Perfusion fluids used in neurosurgery affect cerebrospinal fluid and surrounding brain parenchyma in the rat ventriculocisternal perfusion model

2009 ◽  
Vol 34 (5) ◽  
pp. 511-518 ◽  
Author(s):  
Kazuhisa Doi ◽  
Yujiro Morioka ◽  
Masuhiro Nishimura ◽  
Takeshi Kawano ◽  
Daisuke Harada ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Parenchyma ◽  
Perfusion Model ◽  
Ventriculocisternal Perfusion

scholarly journals The Potential Roles of Blood–Brain Barrier and Blood–Cerebrospinal Fluid Barrier in Maintaining Brain Manganese Homeostasis

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1833
Author(s):  
Shannon Morgan McCabe ◽  
Ningning Zhao
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Blood Circulation ◽  
Critical Role ◽  
Systemic Circulation ◽  
Brain Parenchyma ◽  
Brain Barrier ◽  
Blood Brain ◽  
The Brain

Manganese (Mn) is a trace nutrient necessary for life but becomes neurotoxic at high concentrations in the brain. The brain is a “privileged” organ that is separated from systemic blood circulation mainly by two barriers. Endothelial cells within the brain form tight junctions and act as the blood–brain barrier (BBB), which physically separates circulating blood from the brain parenchyma. Between the blood and the cerebrospinal fluid (CSF) is the choroid plexus (CP), which is a tissue that acts as the blood–CSF barrier (BCB). Pharmaceuticals, proteins, and metals in the systemic circulation are unable to reach the brain and spinal cord unless transported through either of the two brain barriers. The BBB and the BCB consist of tightly connected cells that fulfill the critical role of neuroprotection and control the exchange of materials between the brain environment and blood circulation. Many recent publications provide insights into Mn transport in vivo or in cell models. In this review, we will focus on the current research regarding Mn metabolism in the brain and discuss the potential roles of the BBB and BCB in maintaining brain Mn homeostasis.

Kinetic model for disposition of 6-mercaptopurine in monkey plasma and cerebrospinal fluid

1985 ◽  
Vol 248 (2) ◽  
pp. R147-R156 ◽  
Author(s):  
D. G. Covell ◽  
P. K. Narang ◽  
D. G. Poplack
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Parenchyma ◽  
Lymphocytic Leukemia ◽  
Bolus Administration ◽  
Significant Barrier ◽  
Maintenance Of Remission ◽  
Kinetics Of ◽  
And Diffusion ◽  
Monkey Plasma ◽  
Csf Turnover

The antipurine 6-mercaptopurine (6-MP) is effective in the induction and maintenance of remission in patients with acute lymphocytic leukemia. This report presents a compartmental model that describes the kinetics of 6-MP in the plasma and cerebrospinal fluid (CSF) of the monkey. Analysis is based on simultaneously measured plasma and CSF 6-MP concentrations after intravenous and intraventricular bolus administration. Results indicate that 6-MP administered intraventricularly remains largely in the CSF. Disappearance of 6-MP from CSF is principally due to convective losses at a rate equivalent to CSF turnover. Diffusion of 6-MP across the ependymal surface accounts for only 7% of the 6-MP appearing in the plasma. Conversely the dominant route for entry of 6-MP into the CSF from the plasma is entrainment in choroidally formed CSF. Only 12% of 6-MP in the CSF after intravenous administration can be accounted for by permeation of cerebral capillaries and diffusion through brain parenchyma and across the ependymal surface into CSF. These results indicate that the choroid plexus is not a significant barrier for the transfer of molecules like 6-MP from plasma to CSF.

scholarly journals Porencephalic Cyst in an Adult - A Rare Pathology

2021 ◽  
Vol 10 (12) ◽  
pp. 918-919
Author(s):  
Shreya Tapadia ◽  
Suresh Vasant Phatak ◽  
Harshith Gowda K.B ◽  
Asish Pavanan
Keyword(s):  
Cerebrospinal Fluid ◽  
White Matter ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
Sudden Onset ◽  
Brain Parenchyma ◽  
Motor Deficits ◽  
Cystic Degeneration ◽  
Lateral Side ◽  
Porencephalic Cyst

Porencephalic cyst is a rare entity in adults with limited cases reported so far. It is usually congenital and seen in neonates. Here, we report a 25-year-old male who presented with post-ictal confusion following an episode of sudden onset of generalised tonic clonic seizure. He was diagnosed to have large cerebrospinal fluid (CSF) density cystic lesion in the right parieto-occipital region communicating with occipital horn on right side side of porencephaly. Porencephaly is an uncommon congenital disorder that occurs due to cystic degeneration and encephalomalacia leading to porencephalic cyst formation.1 They are considered to occur most commonly from focal encephalomalacia due to a localised cerebral insult during early gestation, 2 while the other aetiologies include trauma, infection, antenatal intraparenchymal haemorrhage and perinatal cerebral ischemia.3 If the insult occurs in late third trimester it can lead to gliosis. Porencephalic cysts are typically lined by white matter of brain parenchyma.2 They differ widely in their location and size while the clinical manifestations and presentations range from being asymptomatic to extremely impaired mental function. Generally, the signs and symptoms of porencephaly become apparent in the first year of life. The earliest manifestation being spasticity and seizures. As the age increases there is a delay in development of milestones presenting as language impairment, disability in intellect and motor deficits. Clinically head circumference measurement varies from being normal or small to an enlarged head in cases of synechiae formation that creates a one-way valve effect leading to progressive enlargement of the cyst and expansion of skull or there may be hydrocephalus.4 Radiologically the diagnosis depends on demonstrating a well-defined CSF-filled space occupying lesion lined by white matter and communicating with ventricles on computed tomography (CT) scan or magnetic resonance imaging (MRI) of brain. The prognosis of porencephaly depends on the location and extent of the cyst.5 If the cyst is very large it can cause mass effect in the form of scalloping of adjacent bone, buckling of brain parenchyma, midline shift to contra lateral side and hydrocephalus. On MRI, brain cyst appears well defined and lined by white matter with or without gliosis. Cerebrospinal fluid is the content which is shown as hypointense on T1 and hyperintense on T2.

scholarly journals A Case of Brain Herniation and Cerebrospinal Fluid Leakage during Endoscopic Marsupialization of Ethmoid Sinus Mucocele

2020 ◽  
Vol 63 (9) ◽  
pp. 427-431
Author(s):  
Song Jae Lee ◽  
Sang Gyu Park ◽  
Hae Won Choi ◽  
Kyung Rae Kim
Keyword(s):  
Cerebrospinal Fluid ◽  
Surgical Intervention ◽  
Brain Parenchyma ◽  
Ethmoid Sinus ◽  
Sinus Surgery ◽  
Cerebrospinal Fluid Leakage ◽  
Brain Herniation ◽  
Fluid Leakage ◽  
Adjacent Structures ◽  
Ethmoid Sinuses

Paranasal sinus mucocele is a slowly growing benign cystic lesion. It usually involves the frontal and ethmoid sinuses and can extend to adjacent structures, especially to the orbit, skull base and brain parenchyma. Prompt surgical intervention is needed when symptoms occur. Complete resection of mucocele is approached via endoscopic sinus surgery, while marsupialization is also widely considered. Recently, we encountered a case of spontaneous brain herniation and cerebrospinal fluid leakage during endoscopic marsupialization of ethmoid sinus mucocele. Herein, we report the case with a review of the literature.

scholarly journals Selective localization of IgG from cerebrospinal fluid to brain parenchyma

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Marlene Thorsen Mørch ◽  
Sofie Forsberg Sørensen ◽  
Reza Khorooshi ◽  
Nasrin Asgari ◽  
Trevor Owens
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Parenchyma ◽  
Selective Localization

scholarly journals Mechanism of Coup and Contrecoup Injuries Induced by a Knock-Out Punch

2020 ◽  
Vol 25 (2) ◽  
pp. 22 ◽  
Author(s):  
Milan Toma ◽  
Rosalyn Chan-Akeley ◽  
Christopher Lipari ◽  
Sheng-Han Kuo
Keyword(s):  
Cerebrospinal Fluid ◽  
Interaction Model ◽  
Brain Parenchyma ◽  
Primary Objective ◽  
Element Analysis ◽  
Knock Out ◽  
Particle Hydrodynamics ◽  
Smoothed Particle ◽  
The Impact ◽  
The Brain

Primary Objective: The interaction of cerebrospinal fluid with the brain parenchyma in an impact scenario is studied. Research Design: A computational fluid-structure interaction model is used to simulate the interaction of cerebrospinal fluid with a comprehensive brain model. Methods and Procedures: The method of smoothed particle hydrodynamics is used to simulate the fluid flow, induced by the impact, simultaneously with finite element analysis to solve the large deformations in the brain model. Main Outcomes and Results: Mechanism of injury resulting in concussion is demonstrated. The locations with the highest stress values on the brain parenchyma are shown. Conclusions: Our simulations found that the damage to the brain resulting from the contrecoup injury is more severe than that resulting from the coup injury. Additionally, we show that the contrecoup injury does not always appear on the side opposite from where impact occurs.

Effects of inhibitors on chloride outflux from cerebrospinal fluid

1988 ◽  
Vol 64 (5) ◽  
pp. 2183-2189 ◽  
Author(s):  
M. Nishimura ◽  
D. C. Johnson ◽  
H. Kazemi
Keyword(s):  
Cerebrospinal Fluid ◽  
State Level ◽  
Compartment Model ◽  
Disulfonic Acid ◽  
Acid Base Balance ◽  
Quantitative Measurements ◽  
Ventriculocisternal Perfusion ◽  
Base Balance ◽  
Anesthetized Dogs ◽  
The Difference

Movement of chloride from cerebrospinal fluid (CSF) to brain or blood is one of the factors that may be involved in regulation of CSF [Cl-], which is important to CSF acid-base balance. We made quantitative measurements of the unidirectional outflux of radiolabeled chloride (38Cl, half-life 37.3 min) from CSF in anesthetized dogs, using ventriculocisternal perfusion (VCP). The outflux of 38Cl from CSF was determined from the difference between the movements of 38Cl and dextran using a one-compartment model. VCP was performed at a rate of 1.4 ml/min for 14 min, and then slowed to 0.28 ml/min. The 38Cl activity decreased to a steady-state level approximately 12% lower than that of dextran within 40–50 min. Under control conditions for the first run (n = 24), the flux was 0.042 +/- 0.003 (SE) ml/min. The outflux under control conditions (n = 6) tended to increase over three separate determinations in a 6-h period, being 136 +/- 19% of the first run on the second run, and 143 +/- 24% on the third. There were no significant changes in 38Cl outflux compared with control ratios after the inclusion of bumetanide in the VCP fluid (n = 6), which inhibits sodium-coupled Cl- transport, with acetazolamide (n = 6), which inhibits carbonic anhydrase, or with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (n = 6), an inhibitor of carrier-mediated anion exchange. These results suggest that the outward movement of chloride from CSF occurs mostly by passive diffusion and is not by mediated transport.

Afferent vagal stimulation, vasopressin, and nitroprusside alter cerebrospinal fluid kinin

1987 ◽  
Vol 253 (1) ◽  
pp. R136-R141 ◽  
Author(s):  
G. R. Thomas ◽  
H. Thibodeaux ◽  
H. S. Margolius ◽  
J. G. Webb ◽  
P. J. Privitera
Keyword(s):  
Cerebrospinal Fluid ◽  
Vagal Stimulation ◽  
Cardiovascular Regulation ◽  
Perfusion System ◽  
Ventriculocisternal Perfusion ◽  
Anesthetized Dogs ◽  
Bilateral Vagotomy ◽  
Afferent Vagal ◽  
Nitroprusside Infusion ◽  
Stimulation Of

The effects of afferent vagal stimulation, cerebroventricular vasopressin, and intravenous nitroprusside on cerebrospinal fluid (CSF) kinin levels, mean arterial pressure (MAP), and heart rate (HR) were determined in anesthetized dogs in which a ventriculocisternal perfusion system (VP) was established. Following bilateral vagotomy, stimulation of the central ends of both vagi for 60 min significantly increased MAP and CSF perfusate levels of kinin and norepinephrine (NE). MAP was increased a maximum of 32 +/- 4 mmHg, and the rates of kinin and NE appearance into the CSF perfusate increased from 4.2 +/- 1.4 to 22.1 +/- 6.9 and from 28 +/- 5 to 256 +/- 39 pg/min, respectively. A significant correlation was found between CSF kinin and NE levels in these experiments. In other experiments the addition of arginine vasopressin to the VP system caused a significant increase in CSF perfusate kinin without affecting MAP or HR. Intravenous infusion of nitroprusside lowered MAP without affecting kinin levels in the CSF. However, on cessation of nitroprusside infusion, CSF kinin increased significantly in association with the return in MAP to predrug level. Collectively the data are consistent with the hypothesis that central nervous system kinins have some role in cardiovascular regulation, and furthermore that this role may involve an interaction between brain kinin and central noradrenergic neuronal pathways.

Central role for angiotensin in control of adrenal catecholamine secretion

1985 ◽  
Vol 248 (3) ◽  
pp. R363-R370 ◽  
Author(s):  
E. J. Corwin ◽  
J. F. Seaton ◽  
M. Hamaji ◽  
T. S. Harrison
Keyword(s):  
Cerebrospinal Fluid ◽  
Catecholamine Secretion ◽  
Ang Ii ◽  
Artificial Cerebrospinal Fluid ◽  
Ventriculocisternal Perfusion ◽  
Before And After ◽  
Adrenal Response ◽  
Adrenal Secretion ◽  
Lateral Cerebral Ventricle

Angiotensin II (ANG II) is required for unimpaired adrenal reflex secretion of catecholamines after hemorrhage in the dog. To test if ANG II acts centrally, experiments were performed under general anesthesia on bilaterally or sham-nephrectomized dogs hemorrhaged at 25 ml/kg. Ventriculocisternal perfusion of ANG II or its antagonist saralasin was accomplished via needles inserted in the left lateral cerebral ventricle and cisterna magna. Mean arterial pressure and adrenal secretion of catecholamines were measured before and after hemorrhage. Nephrectomized dogs receiving only artificial cerebrospinal fluid (CSF) by ventriculocisternal perfusion had a very small adrenal response to hemorrhage compared with animals receiving ANG II intraventricularly (IVT) (at 10 and 100 pg . kg-1 . min-1). This effect of ANG II IVT also depended on the rate of IVT infusion. Peripheral infusion of ANG II (10 pg . kg-1 . min-1) had no effect on adrenal catecholamine secretion. Animals with intact kidneys given saralasin IVT (0.06 ng/min) responded similarly to nephrectomized dogs receiving only CSF IVT. Intravenous saralasin did not blunt the response to hemorrhage. Thus ANG II appears to support catecholamine secretion via a central mechanism. This mechanism is physiologically significant because either nephrectomy or functional elimination of ANG II by saralasin greatly attenuates the adrenal medullary response to hemorrhage in vivo.

Cerebrospinal fluid transients induced by hypercapnia

1983 ◽  
Vol 245 (5) ◽  
pp. R701-R705
Author(s):  
M. J. Fisher ◽  
S. R. Heisey ◽  
T. Adams ◽  
D. L. Traxinger
Keyword(s):  
Cerebrospinal Fluid ◽  
Formation Rate ◽  
Tracer Concentration ◽  
Perfusion Studies ◽  
Fluid Redistribution ◽  
Ventriculocisternal Perfusion ◽  
Before And After ◽  
Outflow Rate ◽  
The Times ◽  
Stop Flow

Ventriculocisternal perfusion studies using tracers have shown that hypercapnia causes a transient increase in cerebrospinal fluid (CSF) outflow rate (displaced CSF volume, Vd) and a decrease in CSF effluent tracer concentration (tracer-free CSF, CSFtf). This dilution could be due to an increase in CSF formation rate (Vf) and/or to displacement of unequilibrated CSFtf sequestered in poorly mixed compartments. To facilitate convection in the subarachnoid spaces, we used a “stop-flow” procedure (by clamping the cisternal outflow tube while infusion was constant) in anesthetized cats during ventriculocisternal perfusion with mock CSF containing [14C]dextran. Each animal spontaneously breathed air, then 5% CO2 both before and after stopflow. Although Vd and the times over which Vd and CSFtf were defined were unaffected, CSFtf was decreased by 50% after stop-flow. We conclude that during ventriculocisternal perfusion, mixing is incomplete in CSF spaces, and that unequilibrated CSF contributes significantly to the reduced tracer concentration in Vd during acute hypercapnia. To determine whether Vf transiently increases in response to CO2 breathing, or to any perturbation causing craniospinal fluid redistribution, homogeneity in CSF spaces must be verified.

Sign in / Sign up

Export Citation Format

Share Document