Cerebrospinal Fluid Formation Rate in Cold Induced Brain Edema

1980 ◽  
pp. 472-474
Author(s):  
G. M. Hochwald ◽  
K. G. Go
1980 ◽  
Vol 53 (5) ◽  
pp. 652-655 ◽  
Author(s):  
K. Gwan Go ◽  
Gerald M. Hochwald ◽  
Lenie Koster-Otte ◽  
Annie K. van Zanten ◽  
Mysore Gandhi

✓ 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.


1982 ◽  
Vol 60 (8) ◽  
pp. 1138-1143 ◽  
Author(s):  
Betty P. Vogh ◽  
David R. Godman

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.


1999 ◽  
Vol 277 (1) ◽  
pp. R263-R271 ◽  
Author(s):  
C. E. Johanson ◽  
J. Szmydynger-Chodobska ◽  
A. Chodobski ◽  
A. Baird ◽  
P. McMillan ◽  
...  

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.


1976 ◽  
Vol 231 (1) ◽  
pp. 127-131 ◽  
Author(s):  
AN Martins ◽  
TF Doyle ◽  
N Newby

Changes in cerebrospinal fluid formation rate (VF) with hypocapnia were measured by the ventriculocisternal perfusion technique in 24 rhesus monkeys anesthetized with nitrous oxide. In addition cerebral blood flow (CBF) was measured by the hydrogen clearence methods, Vf in control animals declined at a mean rate of 2.3 mul/min each hour during the last 4.5 h of a 7-h perfusion although variables known to effect Vf remained stable. Three hours after perfusion began, Vf of normocapnic controls was 41.4 mul/min +/- 5.4; CBF, 59P ML/100 G PER MIN. When Pco(2) was reduced to half of control, Vf fell to 35.6 mul/min +/- 6.3 and CBF fell by 27%. When Pco(2) was doubled, Vf fell to 33.1 mul/min +/- 5.3 and CBF increased threefold. The difference in Vf id significant only for the hypercapnic group (p=0.01). When animals were used as their own controls, three were no significant differences in Vf with hypercapnia compared to normocapnia. These results indicated that in the monkey variations of Pco(2) within broad physiologic limits, which are sufficient to cause large changes in CBF, have little effect of Vf.


1972 ◽  
Vol 36 (3) ◽  
pp. 276-282 ◽  
Author(s):  
Osamu Sato ◽  
Takahiko Asai ◽  
Yoshiyuki Amano ◽  
Makoto Hara ◽  
Ryuichi Tsugane ◽  
...  

✓ The spinal subarachnoid space of the dog was perfused with an artificial cerebrospinal fluid containing inulin as a tracer. The experimental procedures were based upon the concept that the decrease in inulin concentration occurring during the perfusion was exclusively a function of the volume of newly formed cerebrospinal fluid in the system.


1974 ◽  
Vol 40 (3) ◽  
pp. 381-385 ◽  
Author(s):  
Howard M. Eisenberg ◽  
J. Gordon McComb ◽  
Antonio V. Lorenzo

✓ With the use of a ventricular perfusion technique, a cerebrospinal fluid formation rate of 1.4 ml/min was determined in a 5-month-old child with a choroid plexus papilloma and hydrocephalus. This rate was slightly greater than four times the rate observed in normal children. The clinical course, as well as a measured absorption rate, indicated that the patient's capacity for absorption was normal.


1984 ◽  
Vol 61 (4) ◽  
pp. 707-712 ◽  
Author(s):  
Meihong Cao ◽  
He Lisheng ◽  
Sun Shouzheng

✓ A series of 87 patients with severe brain injury were studied. Intracranial pressure (ICP) monitoring and external ventricular drainage were used to control ICP at high and low levels. Clearance of ytterbium-169-labeled diethylenetriaminepentaacetic acid (169Yb-DTPA), Evans blue dye, and ventricular cerebrospinal fluid protein was measured at the two ICP levels over consecutive periods of 4 hours to confirm clearance of brain edema. The results support the hypothesis that brain edema is in part absorbed in the cerebrospinal fluid via transventricular flow.


1962 ◽  
Vol 4 (0) ◽  
pp. 207b-208
Author(s):  
S. AWAZU ◽  
M. EBARA ◽  
K. AKASHI ◽  
Y. KUSHIDA ◽  
S. MORIMOTO

2000 ◽  
Vol 47 (1) ◽  
pp. 59-64
Author(s):  
T Kryczka ◽  
P Grieb ◽  
M Bero ◽  
J Kasperczyk ◽  
P Dobrzynski

We assessed the rate of release of a model nucleoside (adenosine, 5%, w/w) from nine different lactide-glycolide or lactide-caprolactone polymers. The polymer discs were eluted every second day with an artificial cerebrospinal fluid at the elution rate roughly approximating the brain extracellular fluid formation rate. Adenosine in eluate samples was assayed by HPLC. Three polymers exhibited a relatively constant release of adenosine for over four weeks, resulting in micromolar concentrations of nucleoside in the eluate. This points to the necessity of further development of polymers of this types as intracerebral nucleoside delivery systems for local treatment of brain tumors.


1983 ◽  
Vol 245 (5) ◽  
pp. R701-R705
Author(s):  
M. J. Fisher ◽  
S. R. Heisey ◽  
T. Adams ◽  
D. L. Traxinger

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.


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