Influence of pregnancy on the febrile response to intracerebroventricular administration of PGE1 in rats

Stobie-Hayes, K.M.; Fewell, James E.

doi:10.1152/jappl.1996.81.3.1312

Cited by 24 publications

(18 citation statements)

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“…It is thought that the pyrexia caused by misoprostol is a centrally mediated effect of prostaglandin E 1 [19]. Although pyrexia was more frequent in the misoprostol group in the present study, the difference was not significant.…”

Section: Discussioncontrasting

confidence: 71%

The effect of post‐cesarean rectal misoprostol on intestinal motility

Adanikin

Orji

Fasubaa

et al. 2012

Intl J Gynecology & Obste

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Section: Discussioncontrasting

confidence: 71%

The effect of post‐cesarean rectal misoprostol on intestinal motility

Adanikin

Orji

Fasubaa

et al. 2012

Intl J Gynecology & Obste

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“…Although the data suggested reduced levels of prostaglandins in the brain, we (35) and others (36, 37) have also investigated whether activation of the EP receptors within the brain was equally effective in causing fever throughout late pregnancy and parturition. Body temperature responses to intraventricular PGE 2 were reduced at parturition.…”

Section: Central Nervous System Changes In Pregnancymentioning

confidence: 99%

Suppression of the Febrile Response in Late Gestation: Evidence, Mechanisms and Outcomes

Mouihate

Harré

Martin

et al. 2008

J Neuroendocrinology

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Fever is a beneficial host defence response. However, fever caused by the immune stimulant, lipopolysaccharide (LPS), are attenuated in many species during pregnancy, particularly near term. A number of parallel mechanisms may be responsible, and these vary in magnitude according to the time of gestation, type of inflammatory stimulus and species of animal. Some studies report a reduction in the plasma levels of circulating pro‐inflammatory cytokines such as tumour necrosis factor‐α, interleukin‐1β and interleukin‐6 along with increased levels of anti‐inflammatory cytokines such as interleukin‐1 receptor antagonist. Associated with the attenuated febrile response to LPS is a reduction in the activation of the prostaglandin synthesising enzyme, cyclo‐oxygenase 2, resulting in reduced levels of the obligatory prostaglandin mediators of the febrile response in the brain. There is also a reduction in the sensitivity of the brain to the pyrogenic action of prostaglandins, which does not appear to be due to a change in the levels of hypothalamic EP3 prostaglandin receptors. The suppression of fever at term may be important for the health of the neonate because fever in pregnant mothers may be harmful to the late‐term foetus and neonate.

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“…This febrile refractoriness has been observed in many species, including guinea pig (55), rabbits (28), sheep (14), and rats (7,23,24), and has been observed in response to both peripherally injected pyrogens (14,23,55) and, to a lesser extent, to centrally infused prostaglandins (7,24,48). The fact that fever suppression is most dramatic in response to systemically administered LPS suggests that several steps in the cascade of responses to peripherally injected LPS may be affected.…”

mentioning

confidence: 94%

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Mouihate¹,

Ms²,

Nakamura

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus. Am J Physiol Regul Integr Comp Physiol 283: R800-R805, 2002; 10.1152/ ajpregu.00258.2002The fever response is blunted at near term. As the enzyme cyclooxygenase-2 (COX-2) plays a critical role in fever development, we measured its expression in rat hypothalamus during pregnancy and lactation. Western blot analysis revealed a 72-kDa COX-2-immunoreactive band in non-immune-challenged, pregnant rats at day 15 of pregnancy. In contrast, it was almost undetectable at near term and at lactation day 5. COX-2 was significantly induced at the 15th day of pregnancy and at the 5th lactating day after intraperitoneal lipopolysaccharide (50 g/kg). However, this COX-2 induction was significantly reduced at near term compared with values before and after term. The protein levels of the EP3 receptor in the hypothalamus, one of the prostaglandin E 2 (PGE2) receptors suggested to be a key receptor for fever induction, were unaffected throughout the pregnancy and lactation in both non-immune-challenged and lipopolysaccharide-treated rats. These data suggest that suppression of fever at near term is associated with a significantly reduced induction of COX-2 by lipopolysaccharide, resulting in a reduced production of PGE 2. Altered expression of the EP3 receptor does not seem to be involved in this fever refractoriness at near term.cyclooxygenase-2; parturition; lipopolysaccharide; prostaglandin receptor; EP3 receptor FEVER, A MAJOR PART of host defense, is thought to be of beneficial and adaptive value (15). Thus the inability to develop a fever response to pathogens can be detrimental (16). An absent or reduced fever has been observed in pregnant animals at near term (14) and, in some circumstances, is associated with abortion or mortality (23). This febrile refractoriness has been observed in many species, including guinea pig (55), rabbits (28), sheep (14), and rats (7,23,24), and has been observed in response to both peripherally injected pyrogens (14, 23, 55) and, to a lesser extent, to centrally infused prostaglandins (7,24,48). The fact that fever suppression is most dramatic in response to systemically administered LPS suggests that several steps in the cascade of responses to peripherally injected LPS may be affected.In response to bacterial pyrogens such as LPS, immunocompetent cells generate endogenous cytokines, which signal to the central nervous system through either humoral or neuronal pathways (for review, see Ref. 8) to induce expression of cyclooxygenase-2 (COX-2) (6, 22). The activity of this enzyme results in the cyclooxygenation of arachidonic acid and subsequently the production of PGE 2 , which acts largely in the anterior hypothalamus/preoptic area (47). COX-2 is present in basal conditions in the brain (3, 41), but in inflammation, it is induced specifically in the endothelium of brain capillaries (18,25). Levels of COX-2 have been correlated to levels of PGE 2 during LPS-induced fever (54). Because...

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Influence of pregnancy on the febrile response to intracerebroventricular administration of PGE1 in rats

Cited by 24 publications

References 0 publications

The effect of post‐cesarean rectal misoprostol on intestinal motility

The effect of post‐cesarean rectal misoprostol on intestinal motility

Suppression of the Febrile Response in Late Gestation: Evidence, Mechanisms and Outcomes

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

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