Prostaglandins of the E and F series in rabbit cerebrospinal fluid during fever induced by Newcastle disease virus,E. coli-endotoxin, or endogenous Pyrogen

Philipp-Dormston, W. K.; Siegert, R.

doi:10.1007/bf02123737

Cited by 53 publications

(16 citation statements)

References 14 publications

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“…(see Dey et al 1974), as is the fever caused by the virus of Newcastle Disease (PhilippDormston & Siegert, 1974b). Philipp-Dormston & Siegert (1974b) were the first to show that the fever produced by endogenous pyrogen is also associated with PGE release and our experiments confirm their findings quantitatively.…”

Section: Methodssupporting

confidence: 81%

A dissociation between fever and prostaglandin concentration in cerebrospinal fluid.

Cranston¹,

Hellon²,

Mitchell³

1975

The Journal of Physiology

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SUMMARY1. Sustained fever has been induced in conscious rabbits by i.v. injection and infusion of endogenous pyrogen.2. Cerebrospinal fluid (c.s.f.) was sampled from the cisterna magna at hourly intervals. The concentration of prostaglandin increased in parallel with rectal temperature. The prostaglandin was identified as one of the E series.3. When sodium salicylate (145 m-mole followed by a continuous infusion of 9 /tmole/min) was started 1 hr before endogenous pyrogen, the febrile response to the pyrogen was not significantly diminished but no rise of prostaglandin concentration was detected in c.s.f.4. This dissociation between fever and prostaglandin concentration means that changes in cisternal prostaglandin concentration cannot be accepted as evidence that prostaglandin mediates the febrile response.

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Section: Methodssupporting

confidence: 81%

A dissociation between fever and prostaglandin concentration in cerebrospinal fluid.

Cranston¹,

Hellon²,

Mitchell³

1975

The Journal of Physiology

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“…injections of endogenous pyrogen, a clear distinction between our results and those of previous investigators became apparent. While Philipp-Dormston & Siegert (1974) and Cranston et al (1975b) reported PGE levels which were barely double those of the control values (2-8-4-0 ng/ml. ), we observed on average an almost fivefold increase in the level of PGE in c.s.f.…”

Section: Discussionmentioning

confidence: 66%

“…Perhaps a surprising finding of the study, in the light of previous reports on the increases in PGE levels in c.s.f. of rabbits made febrile by endogenous pyrogen 75 H. A. BERNHEIM, T. J. GILBERT AND J. T. STITT (Philipp-Dormston &Siegert, 1974 andCranston et al 1975b), was the relatively large increases in PGE levels in third ventricular c.s;f. which attended fever production. Both previous investigations reported that control levels of PGE in c.s.f.…”

Section: Discussionmentioning

confidence: 99%

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Prostaglandin E levels in third ventricular cerebrospinal fluid of rabbits during fever and changes in body temperature

Bernheim

Gilbert

Stitt

1980

The Journal of Physiology

118

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1. A method was devised to sample cerebrospinal fluid (c.s.f.) from the third ventricle of conscious rabbits. 2. Levels of PGE were measured in c.s.f. withdrawn from the third ventricle of rabbits exposed to a variety of manipulations of both brain and body core temperatures which mimicked various facets of fever in these animals. These results were compared to the levels of PGE in the c.s.f. of the same rabbits made febrile by I.V. injections of endogenous pyrogen. 3. Levels of PGE in ventricular c.s.f. remained unaltered at 2‐3 ng/ml. during exposure to cold, hyperthermia due to heat exposure, hypothalamic cooling or hypothalamic heating, whereas during fever produced by endogenous pyrogen, they rose to an average of 11‐12 ng/ml. Furthermore, a significant positive correlation was established between the level of PGE measured in the c.s.f. and the subsequent height of the fever produced by the pyrogen. 4. Since production of PGE within the brain is not caused by changes in the brain or body temperatures which are comparable to those observed during fever, and yet greater than fivefold increases in the PGE levels in c.s.f. are produced by I.V. injections of endogenous pyrogen, it is concluded that PGE production in the brain is involved in the pathogenesis of fever.

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“…Secondly, inhibitors of the cyclooxygenase pathway reduced both PGE z concentrations and CSF inflammation in response to pneumococcal challenge. Prostaglandins of the E series are known to induce fever in response to endogenous pyrogen and to increase in concentration in response to challenge of rabbits with Escherichia coli or Shigella endotoxin [8,9]. PGE:z are also known to have direct effects on PMNLs, including inhibition of chemotaxis in response to immune complexes and inhibition of degranulation of leukocytes activated by the chemotactic peptide formylmethionyl-Ieucyl-phenylalanine [10,11].…”

Section: Discussionmentioning

confidence: 99%

Nonsteroidal Anti-Inflammatory Agents in the Therapy for Experimental Pneumococcal Meningitis

Tuomanen

Hengstler

Rich

et al. 1987

Journal of Infectious Diseases

154

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Prostaglandins of the E and F series in rabbit cerebrospinal fluid during fever induced by Newcastle disease virus,E. coli-endotoxin, or endogenous Pyrogen

Cited by 53 publications

References 14 publications

A dissociation between fever and prostaglandin concentration in cerebrospinal fluid.

A dissociation between fever and prostaglandin concentration in cerebrospinal fluid.

Prostaglandin E levels in third ventricular cerebrospinal fluid of rabbits during fever and changes in body temperature

Nonsteroidal Anti-Inflammatory Agents in the Therapy for Experimental Pneumococcal Meningitis

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