scholarly journals Altered formation and bulk absorption of cerebrospinal fluid in FGF-2-induced hydrocephalus

1999 ◽  
Vol 277 (1) ◽  
pp. R263-R271 ◽  
Author(s):  
C. E. Johanson ◽  
J. Szmydynger-Chodobska ◽  
A. Chodobski ◽  
A. Baird ◽  
P. McMillan ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Formation Rate ◽  
Cerebral Aqueduct ◽  
Sprague Dawley ◽  
Main Site ◽  
Bulk Absorption ◽  
The Central Nervous System ◽  
Fluid Formation ◽  
Csf Absorption ◽  
Csf Formation Rate

Upregulation of certain growth factors in the central nervous system can alter brain fluid dynamics. Hydrocephalus was produced in adult Sprague-Dawley rats by infusing recombinant basic fibroblast growth factor (FGF-2) at 1 μg/day into a lateral ventricle for 2, 3, 5, or 10–12 days. Lateral and third ventricular enlargement progressively increased from 2 to 10 days. Ventriculomegaly was also induced by a 75% reduced dose of FGF-2. At 10–12 days, there was a 29% attenuation in cerebrospinal fluid (CSF) formation rate, from 2.5 to 1.8 μl/min ( P < 0.01). Choroid plexus, the main site of CSF secretion, had an augmented number of dark epithelial cells, which have previously been associated with decreased choroidal fluid formation. The twofold elevated resistance to CSF absorption, i.e., 0.8 to 1.7 mmHg ⋅ min−1 ⋅ μl−1, was attributable, at least in part, to enhanced fibrosis and collagen deposits in the arachnoid villi, a major site for CSF absorption. Normal CSF pressure (2–3 mmHg) was consistent with a patent cerebral aqueduct and reduced CSF formation rate. The FGF-2-induced ventriculomegaly is interpreted as an ex vacuuo hydrocephalus brought about by an altered neuropil and interstitium of the brain.

The effect of cold-induced brain edema on cerebrospinal fluid formation rate

1980 ◽  
Vol 53 (5) ◽  
pp. 652-655 ◽  
Author(s):  
K. Gwan Go ◽  
Gerald M. Hochwald ◽  
Lenie Koster-Otte ◽  
Annie K. van Zanten ◽  
Mysore Gandhi
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Formation Rate ◽  
Content Type ◽  
Ventriculocisternal Perfusion ◽  
Fluid Formation ◽  
Csf Formation Rate ◽  
Fine Print

✓ The net contribution of vasogenic brain edema to cerebrospinal fluid (CSF) formation was studied by ventriculocisternal perfusion. Individual cats were perfused both before and 2 ½ hours after a severe cold-induced injury to the cerebral cortex, and the results were compared. Although the edema had occupied the larger part of the hemispheric white matter and bordered the lateral ventricle, a decrease rather than an increase in CSF formation rate was observed. This decrease was related to a decrease in the cerebral perfusion pressure by a regression equation that was not affected by the cold injury.

Na-K activated adenosine triphosphatase formation of cerebrospinal fluid in the cat

1964 ◽  
Vol 206 (5) ◽  
pp. 1165-1172 ◽  
Author(s):  
Thomas S. Vates ◽  
Sjoerd L. Bonting ◽  
W. Walter Oppelt
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Formation Rate ◽  
Cerebral Aqueduct ◽  
Csf Flow ◽  
Atpase System ◽  
Na Ions ◽  
Atpase Inhibition ◽  
Csf Formation Rate

Digitalis-sensitive Na-K activated ATPase (Na-K ATPase), implicated in active cation transport, was shown to occur in cat choroid plexus. Cerebrospinal fluid (CSF) formation rate, measured by collection from cat cerebral aqueduct was inhibited 18% by intravenous desacetyl lanatoside C (0.2 mg/kg). Ouabain, placed intraventricularly, caused inhibition of flow, ranging from 100% by 10–5 mole to 0% by 5 x 10–10 mole. After 10–6 mole ouabain, Na-K ATPase activity in lateral ventricle choroid plexus was inhibited 69% without change in digitalis-insensitive, Mg activated ATPase and carbonic anhydrase activities. Ventriculocisternal perfusion with varying concentrations of ouabain, scillaren A, and hexahydroscillaren A gave CSF flow inhibition (inulin dilution technique) correlating quantitatively with in vitro Na-K ATPase inhibition. Other compounds studied were erythrophleine, cassaine, and l-norepinephrine. It is concluded that the choroid plexus Na-K ATPase system has a primary function in the formation of CSF in the cat, presumably through the active secretion of Na ions into the ventricle.

Cerebrospinal fluid formation in rats and cats during treatment with timolol

1982 ◽  
Vol 60 (8) ◽  
pp. 1138-1143 ◽  
Author(s):  
Betty P. Vogh ◽  
David R. Godman
Keyword(s):  
Cerebrospinal Fluid ◽  
Dose Level ◽  
Aqueous Humor ◽  
Flow Rate ◽  
Formation Rate ◽  
Time Study ◽  
Mean Flow ◽  
Dye Dilution ◽  
Fluid Formation ◽  
The Mean

The influence of timolol upon cerebrospinal fluid formation rate has been examined in rats by the measurement of 22Na+ entry into this fluid after 10, 100, or 1000 μg∙kg−1 i.v, and in cats by the dye-dilution measurement of new fluid formation after 30, or 3000 μg∙kg−1 i.v., or 250 μg∙mL−1 in ventricular perfusate. In rats no change from control rates occurred. In the cats there appeared to be no effect of intraventricular timolol; however, a significant decrease of ~ 25% in the mean flow rate was seen after 40 min when drug was given i.v. at either dose level. A time study showed that no further decrease occurred within 5 h and that the observed decrease continued for at least 3 h. These findings are of interest in view of the ability of topical, intraocular, and i.v. timolol to reduce aqueous humor formation rate.

Development of the brain: a vital role for cerebrospinal fluid

2003 ◽  
Vol 81 (4) ◽  
pp. 317-328 ◽  
Author(s):  
Jaleel A Miyan ◽  
Mohammad Nabiyouni ◽  
Mahjuib Zendah
Keyword(s):  
Cerebrospinal Fluid ◽  
Developmental Process ◽  
Subcommissural Organ ◽  
Third Ventricle ◽  
Cortical Cell ◽  
Vital Role ◽  
Cerebral Aqueduct ◽  
Target Cells ◽  
Main Site

There has been considerable recent progress in understanding the processes involved in brain development. An analysis of a number of neurological conditions, together with our studies of the hydrocephalic Texas (H-Tx) rat, presents an important role for cerebrospinal fluid (CSF) in the developmental process. The fluid flow is essentially one-way and the location of the choroid plexuses in the lateral, third, and fourth ventricles allows for the possibility of new components being added to the fluid at these points. The role of the fourth ventricular CSF is particularly interesting since this is added to the fluid downstream of the cerebral hemisphere germinal epithelium (the main site of cortical cell proliferation and differentiation) and is destined for the basal cisterns and subarachnoid space suggesting different target cells to those within the ventricular system. Moreover, other sources of additions to the CSF exist, notably the subcommissural organ, which sits at the opening of the third ventricle into the cerebral aqueduct and is the source of Reisner's fibre, glycoproteins, and unknown soluble proteins. In this paper a model for the role of CSF is developed from studies of the development of the cortex of the H-Tx rat. We propose that CSF is vital in controlling development of the nervous system along the whole length of the neural tube and that the externalisation of CSF during development is essential for the formation of the layers of neurones in the cerebral cortex.Key words: cerebrospinal fluid, cerebral cortex, development, rat, hydrocephalus.

Maturational differences in acetazolamide-altered pH and HCO3 of choroid plexus, cerebrospinal fluid, and brain

1992 ◽  
Vol 262 (5) ◽  
pp. R909-R914 ◽  
Author(s):  
C. E. Johanson ◽  
Z. Parandoosh ◽  
M. L. Dyas
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Cortex ◽  
Carbonic Anhydrase ◽  
Choroid Plexus ◽  
Intracellular Ph ◽  
Ph Regulation ◽  
Secretory Process ◽  
Sprague Dawley ◽  
Infant Rats ◽  
Fluid Formation

The carbonic anhydrase inhibitor acetazolamide is useful for analyzing ion transport, pH regulation, and fluid formation in developing central nervous system. We used the 14C-labeled dimethadione technique to measure alterations in steady-state pH, and to estimate the HCO3 concentration [HCO3], in choroid plexus (CP), cerebrospinal fluid (CSF), and cerebral cortex of 1- and 3-wk-old Sprague-Dawley rats treated with acetazolamide or probenecid. These drugs can suppress transport of HCO3 and other anions in some cells, consequently altering intracellular pH. In 1-wk-old infant rats whose CSF secretory process is incompletely developed, 1 h of acetazolamide treatment did not significantly change CP intracellular pH or [HCO3]. However, in 3-wk-old rats, in which the ability of CP to secrete ions and fluids is almost fully developed, acetazolamide caused marked increases in CP cell intracellular pH and [HCO3]. In contrast, acetazolamide-induced alkalinization was not observed in CSF or cerebral cortex of the 1- and 3-wk-old animals. The other test agent, probenecid (an inhibitor of anion transport but not of carbonic anhydrase), did not alter the pH of any region at any age investigated. Overall, the results are interpreted in light of developmental changes in carbonic anhydrase and previous findings from kinetic analyses of ion-translocating systems in CP. Acetazolamide may interfere with a CP apical membrane HCO3 extrusion mechanism not fully operational in infant rats.

Cotransport of sodium and chloride by the adult mammalian choroid plexus

1990 ◽  
Vol 258 (2) ◽  
pp. C211-C216 ◽  
Author(s):  
C. E. Johanson ◽  
S. M. Sweeney ◽  
J. T. Parmelee ◽  
M. H. Epstein
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Drug Effects ◽  
Disulfonic Acid ◽  
Base Line ◽  
Sprague Dawley ◽  
Disulfonic Stilbene ◽  
Fluid Formation ◽  
Vitro Analysis

Cerebrospinal fluid formation stems primarily from the transport of Na and Cl in choroid plexus (CP). To characterize properties and modulation of choroidal transporters, we tested diuretics and other agents for ability to alter ion transport in vitro. Adult Sprague-Dawley rats were the source of CPs preincubated with drug for 20 min and then transferred to cerebrospinal fluid (CSF) medium containing 22Na or 36Cl with [3H]mannitol (extracellular correction). Complete base-line curves were established for cellular uptake of Na and Cl at 37 degrees C. The half-maximal uptake occurred at 12 s, so it was used to assess drug effects on rate of transport (nmol Na or Cl/mg CP). Bumetanide (10(-5) and 10(-4) M) decreased uptake of Na and Cl with maximal inhibition (up to 45%) at 10(-5) M. Another cotransport inhibitor, furosemide (10(-4) M), reduced transport of Na by 25% and Cl by 33%. However, acetazolamide (10(-4) M) and atriopeptin III (10(-7) M) significantly lowered uptake of Na (but not Cl), suggesting effect(s) other than on cotransport. The disulfonic stilbene 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 10(-4) M), known to inhibit Cl-HCO3 exchange, substantially reduced the transport of 36Cl. Bumetanide plus DIDS (both 10(-4) M) caused additive inhibition of 90% of Cl uptake, which provides strong evidence for the existence of both cotransport and antiport Cl carriers. Overall, this in vitro analysis, uncomplicated by variables of blood flow and neural tone, indicates the presence in rat CP of the cotransport of Na and Cl in addition to the established Na-H and Cl-HCO3 exchangers.

Atrial natriuretic peptide does not alter cerebrospinal fluid formation in sheep

1992 ◽  
Vol 262 (5) ◽  
pp. R860-R864 ◽  
Author(s):  
A. Chodobski ◽  
J. Szmydynger-Chodobska ◽  
E. Cooper ◽  
M. J. McKinley
Keyword(s):  
Cerebrospinal Fluid ◽  
Atrial Natriuretic Peptide ◽  
Choroid Plexus ◽  
Natriuretic Peptide ◽  
Formation Rate ◽  
Biologically Active ◽  
Dilution Method ◽  
Time Control ◽  
Csf Formation Rate ◽  
Atrial Natriuretic

Because the choroid plexus has been shown to have a high density of atrial natriuretic peptide (ANP) binding sites, we investigated the effect of intracerebroventricular and intravenous administrations of ANP on cerebrospinal fluid (CSF) formation. CSF formation rate was measured in conscious sheep with a dye-dilution method using blue dextran 2000 as an indicator substance. During the experiment animals were partially restrained in a sling, and their ventricular systems were perfused with artificial CSF containing the indicator substance. ANP (alpha-human ANP) administered centrally at rates of 0.015-15 ng/min, resulting in CSF ANP concentrations ranging from physiological to pharmacological CSF hormone levels, was found not to influence CSF formation. Similarly, intravenous administration of ANP at a rate of 10 ng.kg-1.min-1 did not affect CSF formation, i.e., decreases in CSF formation rate in all experiments involving ANP administration were not significantly different from those observed in time control experiments. Our results suggest that ANP does not significantly affect CSF production in sheep. It is possible that the lack of effect of ANP on CSF formation is associated with the predominance in the choroid plexus of clearance receptors over biologically active receptors.

Intracranial pressure, cerebral blood flow, and cerebrospinal fluid formation during hyperammonemia in cat

1986 ◽  
Vol 65 (1) ◽  
pp. 86-91 ◽  
Author(s):  
Adam Chodobski ◽  
Joanna Szmydynger-Chodobska ◽  
Anna Urbańska ◽  
Ewa Szczepańska-Sadowska
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Ammonium Acetate ◽  
Formation Rate ◽  
Ammonia Level ◽  
Blood Ammonia ◽  
Blood Ammonia Level ◽  
Arterial Blood ◽  
Csf Formation Rate

✓ Intracranial pressure (ICP), cerebral blood flow (CBF), and the cerebrospinal fluid (CSF) formation rate were examined in anesthetized cats during ammonia intoxication. Hyperammonemia, evoked by intravenous infusion of ammonium acetate, caused a significant increase in ICP when the arterial blood ammonia level exceeded 400 µmol ⋅ liter−1. A progressive elevation of blood ammonia concentration was followed by a gradual rise in CBF, measured by the xenon-133 clearance technique. At an arterial blood ammonia level exceeding 500 µmol ⋅ liter−1, the CBF reached a plateau at 30% above the mean control value. Increase in ICP correlated weakly, but significantly, with the increase in CBF (R = 0.489, p < 0.005). Elevation of the arterial blood ammonia level to 780.4 ± 25.5 µmol ⋅ liter−1 for 2 hours elicited a significant gradual increase in CSF formation rate, measured by the ventriculocisternal perfusion method with iodine-125-albumin as an indicator substance. A maximum increase in CSF flow of 81% was noted at the end of the ammonium acetate infusion. It is suggested that hyperammonemia increases ICP both by cerebral vasodilatation and by enhancement of the CSF formation rate.

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