Indomethacin blocks the febrile response induced by interleukin-8 in rabbits

1995 ◽  
Vol 269 (6) ◽  
pp. R1469-R1474 ◽  
Author(s):  
A. R. Zampronio ◽  
C. A. Silva ◽  
F. Q. Cunha ◽  
S. H. Ferreira ◽  
I. R. Pela ◽  
...  
Keyword(s):  
Body Temperature ◽  
Intravenous Injection ◽  
Interleukin 8 ◽  
Intracerebroventricular Injection ◽  
Febrile Response ◽  
Limulus Amoebocyte Lysate ◽  
Intracerebroventricular Injections ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Pyrogenic Activity

Interleukin (IL)-8 induces fever in rats by a mechanism independent of the release of cyclooxygenase products. The purpose of this study was to investigate whether a similar mechanism is responsible for the pyrogenic effect of IL-8 in rabbits. Intravenous (0.31-5.0 ng/kg) or intracerebroventricular (15.6-250 pg) injections of IL-8 induced a dose-dependent increase in body temperature. The correlations between the doses of recombinant human IL-8 and the fever index were 0.98 and 0.99 for the intravenous and intracerebroventricular injections, respectively. The pyrogenic activity of IL-8 was not due to contamination with lipopolysaccharide (LPS), inasmuch as the Limulus amoebocyte lysate test showed < 10 pg endotoxin/micrograms IL-8, and boiled IL-8 lost its pyrogenic activity. Indomethacin (2 and 5 mg/kg i.p.) abolished the febrile response induced by the intravenous injection of LPS (5.0 ng/kg), IL-1 beta (5 ng/kg), and IL-8 (5 ng/kg). Indomethacin also abolished the fever induced by the intracerebroventricular injection of IL-8 (62.5 pg) but only partially reduced the response induced by the injection of IL-1 beta (25 pg icv). These results show that, different from rats, indomethacin blocks the febrile response induced by the central or peripheral administration of IL-8 in rabbits.

scholarly journals Effects of anti-inflammatory drugs on fever and neutrophilia induced byClostridium difficiletoxin B

1996 ◽  
Vol 5 (3) ◽  
pp. 183-187 ◽  
Author(s):  
R. A. Cardoso ◽  
A. A. Melo Filho ◽  
M. C. C. Melo ◽  
D. M. Lyerly ◽  
T. D. Wilkins ◽  
...  
Keyword(s):  
Body Temperature ◽  
Clostridium Difficile ◽  
Intravenous Injection ◽  
Febrile Response ◽  
Toxin B ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Dose Dependent Increase ◽  
Dose Dependent

This study investigated the ability ofClostridium difficiletoxin B, isolated from the VPI 10463 strain, to induce fever and neutrophilia in rats. Intravenous injection of toxin B (0.005–0.5 μg/kg) evoked a dose-dependent increase in body temperature. The febrile response to 0.5 μg/kg of the toxin started in 2.5 h, peaked at 5 h, and subsided fully within 24 h. Toxin B also induced a dosedependent neutrophilia. Pretreatment with indomethacin (2 mg/kg, i.p.) did not affect the neutrophilia induced by toxin B, but significantly reduced the febrile response measured 4 to 8 h after toxin B injection. Dexamethasone (0.5 mg/ kg) also markedly diminished the febrile response induced by toxin B. These results show thatClostridium difficiletoxin B induced a febrile response susceptible to inhibition by dexamethasone and indomethacin. Furthermore, they suggest that prostaglandins are not involved in the neutrophilia caused by this toxin.

Interleukin-8 induces fever by a prostaglandin-independent mechanism

1994 ◽  
Vol 266 (5) ◽  
pp. R1670-R1674 ◽  
Author(s):  
A. R. Zampronio ◽  
G. E. Souza ◽  
C. A. Silva ◽  
F. Q. Cunha ◽  
S. H. Ferreira
Keyword(s):  
Body Temperature ◽  
Interleukin 1 ◽  
Interleukin 8 ◽  
Cyclooxygenase Inhibitors ◽  
Interleukin 1 Beta ◽  
Independent Mechanism ◽  
Intracerebroventricular Injections ◽  
Beta 2 ◽  
Dose Dependent ◽  
Pyrogenic Activity

We have studied the mechanism by which interleukin-8 (IL-8) induces fever in rats. Intracerebroventricular injections of IL-8 (5.5-50 ng) evoked dose-dependent increases in body temperature, which reached a plateau 5 h after injection, i.e., later than intracerebroventricular interleukin-1 beta (IL-1 beta; 2 h). The pyrogenic activity of IL-8 was not due to contamination with lipopolysaccharide (LPS) because preincubation of IL-8 with a specific antibody or boiling the IL-8 for 30 min abolished its activity but not that of LPS; also, IL-8 but not LPS induced fever in LPS-tolerant rats. Indomethacin significantly reduced the pyrogenic effects of intracerebroventricular injections of LPS and IL-1 beta but not responses to IL-8, suggesting that pyrogenic responses to IL-8 were mediated independently of prostaglandins. In contrast, dexamethasone markedly attenuated pyrogenic responses to IL-8 and IL-1 beta. These data suggest that inhibition of IL-8 by glucocorticoids contributes to the antipyretic effects of these drugs in fevers resistant to cyclooxygenase inhibitors.

scholarly journals Sleep-promoting effects of endogenous pyrogen (interleukin-1)

1984 ◽  
Vol 246 (6) ◽  
pp. R994-R999 ◽  
Author(s):  
J. M. Krueger ◽  
J. Walter ◽  
C. A. Dinarello ◽  
S. M. Wolff ◽  
L. Chedid
Keyword(s):  
Body Temperature ◽  
Intravenous Injection ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Interleukin 1 ◽  
Cerebral Ventricles ◽  
Endogenous Pyrogen ◽  
Temperature Heating ◽  
Dose Dependent ◽  
Pyrogenic Activity

When infused into the lateral cerebral ventricles of rabbits, human endogenous pyrogen (EP) preparations induced dose-dependent increases in slow-wave sleep concomitant with increasing body temperature. Heating EP to 70 degrees C destroyed its sleep-promoting and pyrogenic activity. Anisomycin (an antipyretic) prevented EP from increasing body temperature without affecting its sleep-promoting activity. Intravenous injection of EP induced fever and transient increases in slow-wave sleep but failed to induce prolonged increases in slow-wave sleep. We conclude that the somnogenic activity of EP is not secondary to its pyrogenic activity.

LH-RH TEST IN 100 PATIENTS WITH OVARIAN INSUFFICIENCY

1974 ◽  
Vol 75 (3) ◽  
pp. 428-434 ◽  
Author(s):  
P.-J. Czygan ◽  
M. Breckwoldt ◽  
F. Lehmann ◽  
R. Langefeld ◽  
G. Bettendorf
Keyword(s):  
Intravenous Injection ◽  
Functional State ◽  
Clear Correlation ◽  
Normal Range ◽  
Ovarian Insufficiency ◽  
Lh Rh ◽  
Dose Dependent Increase ◽  
Dose Dependent

ABSTRACT The effect of synthetic LH-RH was studied in 100 patients with various types of ovarian insufficiency by following up the FSH- and LH-levels in plasma. LH-RH was administered in doses of 12.5, 25 and 100 μg as a rapid intravenous injection. The patients were classified according to the endocrine state of the pituitary as evidenced by the urinary gonadotrophin levels. A clear correlation between the functional state of the pituitary and its responsiveness to exogenous LH-RH was demonstrated. Most of the patients with undetectable low urinary gonadotrophin levels failed to respond. The majority of patients with gonadotrophin excretion in the normal range and those with elevated levels reacted with a dose dependent increase in circulating LH. The amount of liberated FSH however was related to the injected dose only in patients with high gonadotrophic excretion. The present study indicates that synthetic LH-RH provides a useful tool in the evaluation of the pitutiary function particularly in patients with low and with undetectable gonadotrophin excretion. The data presented in this paper also demonstrate that the functional state of the pituitary is clearly reflected by the urinary gonadotrophin levels.

Body temperature response to IL-1 beta in pregnant rats

1995 ◽  
Vol 269 (5) ◽  
pp. R1179-R1182 ◽  
Author(s):  
R. L. Simrose ◽  
J. E. Fewell
Keyword(s):  
Body Temperature ◽  
Intravenous Injection ◽  
Interleukin 1 ◽  
Temperature Response ◽  
Sprague Dawley ◽  
Endogenous Pyrogen ◽  
Febrile Response ◽  
Pregnant Rats ◽  
Sprague Dawley Rats ◽  
Near Term

Rats have an attenuated or absent febrile response to exogenous pyrogen (e.g., bacterial endotoxin) near term of pregnancy. With the aim of providing insight into possible mechanism(s) of the altered febrile response to exogenous pyrogen, experiments have been carried out on 67 time-bred Sprague-Dawley rats to investigate the febrile response to endogenous pyrogen [i.e., interleukin-1 beta (IL-1 beta)]. On day 13 of gestation, intravenous injection of IL-1 beta produced a significant increase in body temperature with a latency of approximately 30 min and a duration of approximately 120 min. In contrast, on days 17 and 21 of gestation as well as on the day of delivery, intravenous injection of IL-1 beta produced significant decreases in body temperature. Thus rats do not develop fever in response to endogenous pyrogen near term of pregnancy but rather become hypothermic. The mechanism of the altered body temperature response to exogenous pyrogen as pregnancy proceeds remains unknown. We speculate, however, that it most likely lies downstream from the formation of endogenous pyrogen.

Fever and antipyresis in the lizard Dipsosaurus dorsalis

1976 ◽  
Vol 231 (1) ◽  
pp. 198-203 ◽  
Author(s):  
HA Bernheim ◽  
MJ Kluger
Keyword(s):  
Body Temperature ◽  
Aeromonas Hydrophila ◽  
Sodium Salicylate ◽  
Natural Habitat ◽  
The United States ◽  
University Of Michigan ◽  
Febrile Response ◽  
Dipsosaurus Dorsalis ◽  
The University ◽  
Dose Dependent

Lizards (Dipsosaurus dorsalis) were placed in a desertlike environment in which the ambient temperature (Ta) at night (1800-0600 h) was 12 degrees C and the day (0600-1800 h) Ta was between 30 and 55 degrees C depending on the location within the chamber. When dead Aeromonas hydrophila (4 X 10(9) organisms) was injected into nine lizards, an elevation in body temperature (Tb) of 2.7 degrees C was observed during the same day. On the day after bacterial injection the lizards' body temperatures averaged 41.6 degrees C, an increase of 4.2 degrees C over their control day Tb. Further investigations on the febrile response of D. dorsalis were conducted at the University of Wisconsin's Biotron, where there exists a simulated desert environment with the light intensity, temperature, and humidity closely parelleling a typical spring day in the southwestern desert of the United States (the natural habitat of Dipsosaurus). In this environment injection of dead bacteria into seven lizards led to an average febrile response of similar magnitude (Tb = 40.5 degrees C) but with a longer latency than that found at the University of Michigan. Injection of 13 lizards with live A. hydrophila (5 X 10(9) organism subcut.) in the simulated desert at Michigan led to a daytime fever averaging 2.3 degrees C (mean Tb = 40.6 degrees C) over a 5-day period. During the 6th and 7th day the lizards' body temperature returned to the normal or afebrile level. Injections of sodium salicylate along with dead A. hydrophila resulted in a dose-dependent attenuation of the febrile response. These results demonstrate that the reptilian febrile response is strikingly similar to avian and mammalian fever and suggest a common origin and perhaps function for the febrile mechanism.

Interaction between norepinephrine and prostaglandin E2 in the preoptic area of guinea pigs

1996 ◽  
Vol 271 (3) ◽  
pp. R528-R536 ◽  
Author(s):  
E. Sehic ◽  
A. L. Ungar ◽  
C. M. Blatteis
Keyword(s):  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Prostaglandin E2 ◽  
Intravenous Injection ◽  
Guinea Pigs ◽  
Preoptic Area ◽  
Extracellular Fluid ◽  
Low Ph ◽  
Febrile Response ◽  
Artificial Cerebrospinal Fluid

The release of norepinephrine (NE) and prostaglandin E2 (PGE2) in the preoptic-anterior hypothalamus (POA) by systemically administered pyrogens suggests that both substances may mediate the febrile response. To investigate their possible interaction, we measured directly the levels of PGE2 in the extracellular fluid of the POA of conscious guinea pigs microdialyzed intrapreoptically with exogenous NE over the entire course of their febrile response to endotoxin. Acidified and buffered NE (NEa, NEb), artificial cerebrospinal fluid (aCSFa, aCSFb), and vehicle (Veha, Vehb) were tested. All but aCSFb depressed the febrile response to endotoxin. The microdialysis of aCSFa, aCSFb, Veha, Vehb, and NEa did not change basal preoptic PGE2 levels. However, NEb, at a dose that by itself did not affect body temperature (Tb), caused a large elevation in preoptic PGE2. The intravenous injection of endotoxin increased the level of PGE2 in the POA. NEb potentiated this increase, whereas NEa, aCSFa, and Vehb reduced it; Veha reduced it for the first 60 min and enhanced it for the last 90 min of the experiment. Thus these data suggest that the low pH of the NE solute and/or its Veh may confound the observed effects of NE on the Tb and preoptic PGE2 induced by endotoxin. We surmise that this is due to a neurotoxic action of the antioxidants and the acidity of the solution on thermosensitive neurons in the POA. Hence, the results of experiments using exogenous, usually acidified, NE preparations that often also contain additives should be interpreted with caution.

Central and peripheral administration of endothelin-1 induces an increase in blood pressure in conscious trout

1999 ◽  
Vol 276 (4) ◽  
pp. R1010-R1017 ◽  
Author(s):  
Jean-Claude le Mével ◽  
Catherine Delarue ◽  
Dominique Mabin ◽  
Hubert Vaudry
Keyword(s):  
Blood Pressure ◽  
Plasma Cortisol ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Plasma Cortisol Level ◽  
Intracerebroventricular Injection ◽  
Aortic Blood ◽  
Aortic Blood Pressure ◽  
Dose Dependent Increase ◽  
Dose Dependent

The central and peripheral cardiovascular effects of endothelin (ET)-1 and ET-3 were investigated in conscious rainbow trout. Both intracerebroventricular and intra-arterial injections of ET-1 (6.25–25 pmol) but not ET-3 (25 pmol) caused a dose-dependent increase in mean dorsal aortic blood pressure and a concomitant decrease in heart rate. The hypertensive effects induced by intra-arterial and intracerebroventricular injection of ET-1 were associated with a significant ( P < 0.05) increase in systemic vascular resistance. Intracerebroventricular injection of ET-1 induced a twofold higher pressor response than that caused by intra-arterial injection of ET-1 and provoked a barostatic gain that was reduced by 2.5- to 3-fold compared with that calculated after intra-arterial administration of the peptide. The ET receptor antagonist bosentan significantly ( P< 0.05) attenuated these responses regardless of the route of administration. Finally, intra-arterial injection of ET-1 did not significantly modify plasma cortisol level. The present data demonstrate that intracerebroventricular and intra-arterial administration of very low doses of ET-1 produces hypertension in conscious trout. The lack of effect of ET-3 indicates that the hemodynamic actions of ET-1 are mediated both centrally and peripherally through ETAreceptors.

Effect of indomethacin on febrile response to recombinant human interleukin 1-alpha in rabbits

1988 ◽  
Vol 255 (4) ◽  
pp. R527-R533 ◽  
Author(s):  
M. Hashimoto ◽  
T. Bando ◽  
M. Iriki ◽  
K. Hashimoto
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Potent Inhibitor ◽  
Interleukin 1 ◽  
Febrile Response ◽  
Small Rise ◽  
The Central Nervous System ◽  
Colonic Temperature ◽  
Dose Dependent Increase ◽  
Dose Dependent

Effects of indomethacin, a potent inhibitor of prostaglandin (PG) synthesis, on the fever induced by recombinant human interleukin 1-alpha (rhIL 1-alpha) was studied in conscious rabbits. Intracerebroventricularly administered rhIL 1-alpha induced a dose-dependent increase in colonic temperature that was prominently suppressed by pretreatment with indomethacin given either intracerebroventricularly or subcutaneously. On the other hand, fever induced by intravenous administration of rhIL 1-alpha was not completely suppressed by either subcutaneous or intracerebroventricular indomethacin; a small rise in colonic temperature persisted at approximately 45 min after rhIL 1-alpha injection. This rise in colonic temperature was suppressed when indomethacin was given both intracerebroventricularly and subcutaneously. It is suggested that PGs synthesized in the central nervous system contribute to the IL 1 fever and that part of IL 1-alpha given peripherally is also transmitted into the central nervous system to contribute to IL 1 fever.

scholarly journals Characterization of the Physiological Response followingIn VivoAdministration ofAstragalus membranaceus

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Karen Denzler ◽  
Jessica Moore ◽  
Heather Harrington ◽  
Kira Morrill ◽  
Trung Huynh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Dynamic Change ◽  
Baseline Values ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

The botanical,Astragalus membranaceus, is a therapeutic in traditional Chinese medicine. Limited literature exists on the overallin vivoeffects ofA. membranaceuson the human body. This study evaluates the physiological responses toA. membranaceusby measuring leukocyte, platelet, and cytokine responses as well as body temperature and blood pressure in healthy individuals after thein vivoadministration ofA. membranaceus. A dose-dependent increase in monocytes, neutrophils, and lymphocytes was measured 8–12 hours after administration and an increase in the number of circulating platelets was seen as early as 4 hours. A dynamic change in the levels of circulating cytokines was observed, especially in interferon-γand tumor necrosis factor-α, IL-13, IL-6, and soluble IL-2R. Subjective symptoms reported by participants were similar to those typically experienced in viral type immune responses and included fatigue, malaise, and headache. Systolic and diastolic blood pressure were reduced within 4 hours after administration, while body temperature mildly increased within 8 hours after administration. In general, all responses returned to baseline values by 24 hours. Collectively, these results support the role ofA. membranaceusin priming for a potential immune response as well as its effect on blood flow and wound healing.

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