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

Abstract

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 Levels of PGE were measured in c.s.f. withdrawn from the third ventricle of rabbits exposed to a variety of manipulations of both brain and body core temperatures which mimicked various facets of fever in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.

Cytokine inhibitors and pain control

“…In turn, this cytokine induces the production of other inflammatory mediators (36) . The demonstration that IL-1β stimulates the production of prostaglandins (37,38) and that prostaglandins ultimately sensitize the nociceptor (39,40) , prompted the investigation of the IL-1β hypernociceptive role and mechanism. In a seminal finding, it was demonstrated the IL-1β importance to the genesis of inflammatory hypernociception in experimental animals (22) .…”

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

“…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].…”

Anti-inflammatory, analgesic, and antipyretic activities of virgin coconut oil

“…Yeasts, exogenous pyrogens, are capable of stimulating the release of endogenous pyrogens (interleukin-1 and tumor necrosis factor) from polymorphonuclear leukocytes, monocytes, and other cells. These pyrogens act on the thermoreceptive region in the preoptic anterior hypothalamus to release arachidonic acid, stimulate PG synthesis, and raise the set point of the temperature-regulating center, which leads an to increase of body temperature (Bernheim et al, 1980;Kadar, 1998;Kumar et al, 2005). Ibuprofen, a nonsteroidal anti-inflammatory agent, possesses antipyretic activity by inhibiting cyclooxygenase and thus blocking the synthesis or release of PGs in the thermoregulatory center (Wagner et al, 2004;Kumar et al, 2005).…”