The effect of intraventricular air on the rate of cerebrospinal fluid formation in dogs

1972 ◽  
Vol 37 (2) ◽  
pp. 177-181 ◽  
Author(s):  
Michael D. F. Deck ◽  
V. Deonarine ◽  
D. Gordon Potts

✓ Experiments were performed on dogs to estimate the effect of intraventricular air on the rate of cerebrospinal fluid formation. The rate of formation was measured satisfactorily in eight beagle dogs before and after the introduction of air using ventriculocisternal perfusion of artificial cerebrospinal fluid containing 14C-labelled inulin. Statistical analysis of rates of cerebrospinal fluid formation estimated half hourly indicated that there was little or no change after the introduction of air.

1974 ◽  
Vol 41 (3) ◽  
pp. 350-355 ◽  
Author(s):  
Michael E. Carey ◽  
A. Richard Vela

✓The rate of cerebrospinal fluid (CSF) production in dogs was measured by ventriculocisternal perfusion with artificial CSF containing inulin. In normotensive animals, the average CSF production was 36 ± 6 µl/min. When the mean arterial blood pressure was reduced to 62 ± 1 mm Hg, the CSF production fell to 22 ± 5 µl/min, a 39% reduction in fluid formation. The authors briefly discuss various hypotheses to explain this reduction.


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.


1975 ◽  
Vol 42 (6) ◽  
pp. 674-678 ◽  
Author(s):  
Warren E. Lux ◽  
Joseph D. Fenstermacher

✓ The authors perfused rhesus monkeys from lateral ventricles to lumbar sac with an artificial cerebrospinal fluid (CSF) containing a Blue Dextran 2000 marker. Analysis of marker dilution at steady state showed ventricular CSF formation occurring at a rate of 28.3 ± 2.5 µ1/min. No significant CSF formation was found in the spinal subarachnoid space.


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.


1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.


1973 ◽  
Vol 38 (2) ◽  
pp. 167-171 ◽  
Author(s):  
Darwin J. Ferry ◽  
Ronald Gooding ◽  
Jim C. Standefer ◽  
G. Michael Wiese

✓ Cerebrospinal fluid (CSF) changes induced by Pantopaque myelography were determined by comparing samples of CSF from 47 patients with disc symptoms, obtained before and after myelography. Cell count, total protein, colloidal gold curve, and CSF protein electrophoretic patterns were compared. An immediate and persistent modest lymphocytosis was found. Total protein and CSF gamma globulin were elevated 3 weeks after myelography and throughout the remainder of the 80-day study period. This CSF profile characterizes a chronic inflammatory reaction induced by Pantopaque.


1985 ◽  
Vol 248 (3) ◽  
pp. R363-R370 ◽  
Author(s):  
E. J. Corwin ◽  
J. F. Seaton ◽  
M. Hamaji ◽  
T. S. Harrison

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.


1983 ◽  
Vol 59 (3) ◽  
pp. 369-383 ◽  
Author(s):  
J. Gordon McComb

✓ Recent information regarding the nature of bulk cerebrospinal fluid formation and absorption is reviewed, integrated with previous knowledge, and applied to the clinical setting.


1971 ◽  
Vol 34 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Alfonso Schettini ◽  
Lachlan McKay ◽  
Raymond Majors ◽  
Joseph Mahig ◽  
Arnold H. Nevis

✓ A method for monitoring brain surface pressure through the intact dura has been designed based upon the concept of a coplanar, non-sensitive ring transducer. The transducer detects the underlying brain pressure while the stretching forces of the dural membrane are dissipated at the outer ring. The strain gauge consists of a piezo-resistive silicon-chip sensing element and a dummy element that provides temperature compensation. Cisternal cerebrospinal fluid (CSF) and brain surface pressures were monitored simultaneously in dogs under general anesthesia, both before and after increased intracranial pressure was produced experimentally. A difference was found between CSF and brain surface pressures. Possible explanations for this observation are discussed.


1978 ◽  
Vol 48 (5) ◽  
pp. 754-764 ◽  
Author(s):  
Hans J. Reulen ◽  
Matsutaira Tsuyumu ◽  
Anne Tack ◽  
Andreas R. Fenske ◽  
George R. Prioleau

✓ The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I131 and sucrose-C14 labeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternal perfusion. The effect of low- or high-pressure perfusion on edema spread was determined by measuring the water, sodium, RISA-I131, and sucrose-C14 content of serial tissue blocks taken from the injured cortex through the white matter to the ventricular ependyma. The findings indicate that increasing the hydrostatic pressure gradient between edematous brain and CSF enhances the clearance of edema fluid into the ventricular CSF. This was conclusively demonstrated with low-pressure ventricular perfusion which markedly diminished the amount of edema close to the ventricles compared to the controls. The concentration of albumin, sodium, and potassium in the fluid removed from the tissue during low-pressure perfusion indicates that bulk flow was the primary method of edema movement through the extracellular space. With high-pressure perfusion the concentration profiles suggested alternative mechanisms of edema resolution, such as diffusion and reabsorption into capillaries.


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