Further evidence implicating prostaglandin E2 in the genesis of pyrogen fever

1988 ◽  
Vol 254 (3) ◽  
pp. R463-R469 ◽  
Author(s):  
F. Coceani ◽  
J. Lees ◽  
I. Bishai

Conscious cats were used to study the effects of endotoxin and interleukin 1 (IL 1) on levels of prostaglandin (PG) E2 and thromboxane (TX) B2 (the stable TXA2 byproduct) in cerebrospinal fluid (CSF) from the third ventricle. Pyrogens were given intravenously or intraventricularly and prostanoids were measured by radioimmunoassay. PGE2 was normally less abundant than TXB2 (mean, 37 vs. 528 pg/ml), and its level increased severalfold during the sustained fever following intravenous endotoxin (bolus) or IL 1 (bolus plus infusion). PGE2 elevation preceded the fever and was maintained thereafter. Likewise, intraventricular pyrogens promoted PGE2 formation, and their effect was also manifest during the latent period of the fever. The PGE2 metabolite, 13,14-dihydro-15-keto-PGE2, was not measurable in CSF from either afebrile or febrile animals. Basal content of PGE2, on the other hand, was higher in animals pretreated with probenecid (30 mg/kg ip or iv; 50 or 100 micrograms ivt), confirming the importance of transport processes in removing prostanoids from brain. Unlike PGE2, TXB2 levels did not change during the fever to intravenous endotoxin. TXB2 rose instead in response to intraventricular endotoxin, although the elevation did not extend beyond fever uprise. Furthermore, a TXA2 analog (ONO-11113;2 or 4 micrograms ivt) had inconsistent effects on body temperature, while a TXA2 antagonist (ONO-11120;2 micrograms ivt) did not interfere with endotoxin fever. These findings strongly support a causative role for PGE2 in the onset and progression of pyrogen fever. No evidence of a similar role was obtained for TXA2.

1961 ◽  
Vol 37 (4) ◽  
pp. 559-564 ◽  
Author(s):  
Nils Norman

ABSTRACT Two artificial cerebrospinal fluid mixtures, one having a higher than normal sodium, but lower than normal potassium content, the other having a lower than normal sodium, but higher than normal potassium content, were perfused alternately through the cerebral ventricular system of seven dogs, from the right lateral ventricle and down through the third ventricle, aqueduct and fourth ventricle. During this procedure blood was collected through the adrenal vein and the concentration of cortisol (11β, 17,12-trihydroxy-pregn-4-eme-3,20-dione), cortisone (17,21-dihydroxypregn-4-ene-3,11.20-trione), corticosterone (11β,21-dihydroxy-pregn-4-ene3,20-dione). compound S (11-dihydroxy-3,20-dioxo-pregn-4-en-18-al) and aldosterone (11β.21-dihydroxy-3,20-dioxo-pregn-4-en-18-al) determined. A gradual and marked increase in the secretion of all the cortical compounds was observed during the procedure. This pattern was not altered by changing from one of the artificial cerebrospinal fluid mixtures to the other.


1983 ◽  
Vol 244 (6) ◽  
pp. R785-R793 ◽  
Author(s):  
F. Coceani ◽  
I. Bishai ◽  
C. A. Dinarello ◽  
F. A. Fitzpatrick

Levels of prostaglandin (PG) E2 and thromboxane (TX) B2, the stable metabolite of TXA2, were measured by radioimmunoassay in cerebrospinal fluid (CSF) collected from the third ventricle and the cisterna magna of conscious cats. In the absence of fever, PGE2 was usually below the threshold of the assay (0.05-0.37 ng/ml), while TXB2 was measurable in the majority of cases and its concentration was greater in the third ventricle (about 0.7 ng/ml) than in the cisterna magna (about 0.2 ng/ml). At either site, TXB2 content rose if any manipulation was required for the collection of samples. PGE2 levels increased to measurable values (max 1.1-1.4 ng/ml) during fever produced by intrathecal or intravenous administration of leucocytic pyrogen. In contrast, TXB2 concentration rose to an average of 2.2-4 ng/ml only when pyrogen (bacterial or leukocytic) was given intrathecally. Moreover, TXB2 elevation, unlike PGE2 elevation, was limited to the uprise phase of the fever. Imidazole, given either intraperitoneally (50 mg/kg) or intrathecally (3 mg), attenuated the pyrogen fever and suppressed any rise in TXB2 levels. At the same time, the drug tended to increase the PGE2 content of the CSF. Evidence was also obtained suggesting that a fraction of PGE2 is bound to CSF protein, and this event may be important to the inactivation of the compound. These findings are consistent with the concept that PGE2 is involved in the sequence of events underlying pyrogen fever. A role for thromboxane A2 in this process remains to be established.


1972 ◽  
Vol 50 (11) ◽  
pp. 1066-1071 ◽  
Author(s):  
K. E. Cooper ◽  
W. L. Veale

An injection of paraffin oil into the lateral cerebral ventricle of afebrile rabbits appears to fill the entire ventricular system. Such an injection does not affect body temperature nor does it alter the time elapsing between an intravenous injection of leucocyte pyrogen and the fever which follows. It does, however, greatly increase the height and duration of the fever. Oil injected into the cerebral ventricles of rabbits during an intravenous infusion of pyrogen in an amount previously shown to maintain a steady fever level causes the body temperature to commence to climb again and continue to climb considerably thereafter. We suggest that these experiments indicate that leucocyte pyrogen, reaching the hypothalamus via the blood stream, may be excreted through the ependyma of the third ventricle into the cerebrospinal fluid, or that substances released as a result of the presence of leucocyte pyrogen in brain tissue may be thus excreted.


2010 ◽  
Vol 58 (1) ◽  
pp. 156 ◽  
Author(s):  
Chandrasekharan Kesavadas ◽  
TirurRaman Kapilamoorthy ◽  
Gireesh Menon ◽  
KythasandraShivakumar Deepak

1983 ◽  
Vol 245 (4) ◽  
pp. R541-R548 ◽  
Author(s):  
C. Simon-Oppermann ◽  
D. Gray ◽  
E. Szczepanska-Sadowska ◽  
E. Simon

A device for chronic implantation was developed that allowed sampling of cerebrospinal fluid (CSF) from the anterior part of the third cerebral ventricle (A3V) of dogs in repeated experiments for up to 4 mo. Osmolalities, electrolyte concentrations, and concentrations of arginine vasopressin (AVP) measured with a radioimmunoassay were determined in repeated experiments on the chronically prepared animals under conditions of normal hydration, both in the conscious state and during inhalation anesthesia. In conscious dogs, AVP concentrations in plasma and CSF were 3.3 +/- 0.4 and 21.8 +/- 2.5 pg X ml-1, respectively. During anesthesia without surgical interference, the AVP concentrations in plasma and CSF were increased twofold above the levels obtained in conscious dogs. During the time of observation (180 min) all measured parameters remained constant. The AVP concentrations in plasma and CSF samples collected during the surgical procedure of device implantation were about 10-fold higher than in the samples collected during the conscious state. Thus, in each experimental condition, AVP concentration in the CSF collected from the A3V was consistently higher than that in the simultaneously collected blood samples.


1962 ◽  
Vol 40 (1) ◽  
pp. 1811-1818 ◽  
Author(s):  
Catherine F. C. MacPherson

Experiments are described which have led to the standardization of a procedure for the purification of the γc globulin characteristic of cerebrospinal fluid (CSF). The procedure involves the stepwise elution of three chromatographic fractions from a DEAE column by TRIS–HCl buffers at pH 8.5. The composition of the fractions will vary with the relative concentration of the γc globulin in the CSF applied to the column. From an average CSF pool the first fraction, F1, eluted by 0.002 M TRIS–HCl will usually contain only the γc globulin. The second fraction F2, eluted by 0.02 M TRIS-HCl, will contain a mixture of the γc, γs, and βc globulins. The third fraction F3, eluted by 0.08 M TRIS–HCl, will contain chiefly γs globulin as well as traces of the γc and βc globulins. Most of the γc globulin from pooled CSF may then be obtained in purified form by rechromatographing the F2's from several runs. Almost all of the γc globulin applied will be found in F1. The γs and βc globulins will be eluted in the other two fractions.


1977 ◽  
Vol 14 (2) ◽  
pp. 138-145 ◽  
Author(s):  
R. W. Cook

A 10-month-old female, Wire-haired Pointing Griffon dog had a hamartoma of the hypothalamus. Episodes of sudden flaccid collapse had increased in frequency and duration for 7 months. Cerebrospinal fluid pressure was normal. A flat, pedunculated mass, 2.5×3.0×0.9 cm, covered the brain stem between the pituitary gland and pons. Its 1.2-cm-diameter connection to the hypothalamus obliterated the mammillary bodies and extended to the tuber cinereum, distorting the hypothalamus and displacing the third ventricle which also divided the rostral part of the mass. The tissue of the hamartoma resembled gray matter with bullous cytoplasmic vacuolation of many neurons, spongiform change, gemistocytosis and microscopic foci of calcification.


2002 ◽  
Vol 92 (3) ◽  
pp. 975-981 ◽  
Author(s):  
Renata C. H. Barros ◽  
Luiz G. S. Branco

Hypoxia causes hyperventilation and decreases body temperature (Tb) and metabolism [O2 consumption (V˙o 2)]. Because dopamine (DA) is released centrally in response to peripheral chemoreceptor stimulation, we tested the hypothesis that central DA mediates the ventilatory, thermal, and metabolic responses to hypoxia. Thus we predicted that injection of haloperidol (a DA D2-receptor antagonist) into the third ventricle would augment hyperventilation and attenuate the drop in Tb and V˙o 2 in conscious rats. We measured ventilation, Tb, andV˙o 2 before and after intracerebroventricular injection of haloperidol or vehicle (5% DMSO in saline), followed by a 30-min period of hypoxia exposure. Haloperidol did not change Tb orV˙o 2 during normoxia; however, breathing frequency was decreased. During hypoxia, haloperidol significantly attenuated the falls in Tb andV˙o 2, although hyperventilation persisted. The present study shows that central DA participates in the thermal and metabolic responses to hypoxia without affecting hyperventilation, showing that DA is not a common mediator of this interaction.


1986 ◽  
Vol 65 (3) ◽  
pp. 401-403 ◽  
Author(s):  
Abdel Wahab M. Ibrahim ◽  
Hisham Farag ◽  
Mohammed Naguib ◽  
Ezzeldin Ibrahim

✓ Colloid cysts of the third ventricle are described in middle-aged twin brothers. One of them presented with recurrent attacks of headache. In this patient the cyst had reached a size large enough to obstruct the cerebrospinal fluid pathway, resulting in hydrocephalus. The twin brother, although asymptomatic, was suspected of the anomaly and investigated because of the similarity of his ocular signs. The diagnosis was confirmed by computerized tomography in both the patient and his brother. The latter proved to have a smaller colloid cyst situated anteriorly in the third ventricle with no obstructive hydrocephalus. The patient was successfully operated on, while the brother is still under observation. Both brothers have had bilateral cataracts, retinal detachments, and left lateral rectus palsies. The familial occurrence of colloid cysts and their association with these ocular findings have apparently not been described before.


1989 ◽  
Vol 256 (3) ◽  
pp. R674-R684 ◽  
Author(s):  
E. Arnauld ◽  
V. Bibene ◽  
J. Meynard ◽  
F. Rodriguez ◽  
J. D. Vincent

The effect of arginine vasopressin (AVP) on the duration and the relative proportion of sleeping and wakeful periods has been investigated. Vigilance states were determined by visual scoring of polygraphic recordings from unrestrained rats. Animals were implanted with a cannula into the third ventricle through which AVP or related drugs, dissolved in artificial cerebrospinal fluid, were infused at a constant rate by an osmotic pump. Polygraphic data were collected 24 h/day from day 4 to day 9. Recordings were continued for 3 additional days during AVP recovery. AVP infusions significantly increased the amount of time spent in waking compared with control or recovery periods (12%). This effect was mimicked by an AVP agonist (2-phenylalanine, 8-ornithine oxytocin). Oxytocin, a peptide structurally close to AVP, induced a mild change in waking time. The infusion of an AVP antagonist, 1-desaminopenicillamine-2-(O-methyl)tyrosine-arginine vasopressin (dPTyr(Me)AVP), or of anti-AVP antibodies significantly decreased duration of waking. The infusion of antioxytocin antibodies did not modify the duration of waking. The effects of structural analogues of AVP relatively specific for each type of peripheral AVP receptor indicated the participation of a V1-like AVP receptor in the action of AVP on waking time. During infusion of anti-AVP antibodies and dPTyr(Me)AVP and during the first days of recovery from AVP infusion, the ultradian rhythmic distribution of sleep and wakefulness was still present, but the amplitude of the circadian rhythm was reduced.


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