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.

Evidence that platelet-derived growth factor may be a novel endogenous pyrogen in the central nervous system

2000 ◽  
Vol 278 (5) ◽  
pp. R1275-R1281 ◽  
Author(s):  
Irene R. Pelá ◽  
Márcia E. S. Ferreira ◽  
Miriam C. C. Melo ◽  
Carlos A. A. Silva ◽  
Márcio M. Coelho ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Growth Factor ◽  
Third Ventricle ◽  
Platelet Derived Growth Factor ◽  
Febrile Response ◽  
The Central Nervous System ◽  
Factor Α ◽  
Colonic Temperature

Platelet-derived growth factor (PDGF) exerts neurotrophic and neuromodulatory actions in the mammalian central nervous system (CNS). Like the cytokines, PDGF primarily signals through tyrosine phosphorylation-dependent pathways that activate multiple intracellular molecules including Janus family kinases. We previously showed that microinjection of PDGF-BB into the lateral ventricle induced a febrile response in rats that was reduced by pretreatment with Win 41662, a potent inhibitor of PDGF receptors (Pelá IR, Ferreira MES, Melo MCC, Silva CAA, and Valenzuela CF. Ann NY Acad Sci 856: 289–293, 1998). In this study, we further characterized the role of PDGF-BB in the febrile response in rats. Microinjection of PDGF-BB into the third ventricle produced a dose-dependent increase in colonic temperature that peaked 3–4 h postinjection. Win 41662 attenuated fever induced by intraperitoneal injection of bacterial lipopolysaccharide, suggesting that endogenous PDGF participates in the febrile response to this exogenous pyrogen. Importantly, febrile responses induced by tumor necrosis factor-α, interleukin-1β, and interleukin-6 were unchanged by Win 41662. Both indomethacin and dexamethasone blocked the PDGF-BB-induced increase in colonic temperature, and, therefore, we postulate that PDGF-BB may act via prostaglandin- and/or inducible enzyme-dependent pathways. Thus our findings suggest that PDGF-BB is an endogenous CNS mediator of the febrile response in rats.

Centrally administered ouabain aggravates central sleep apneas

1993 ◽  
Vol 74 (2) ◽  
pp. 545-548 ◽  
Author(s):  
T. Sato ◽  
M. Tadokoro ◽  
H. Kaba ◽  
H. Saito ◽  
K. Seto ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Eye Movement ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
The Central Nervous System ◽  
Freely Moving ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Lateral Cerebral Ventricle

The presence of endogenous digitalis-like factors in the central nervous system suggests their functional significance in the central nervous system. Three-day infusions of three-stepped doses of the digitalis agent ouabain (1–100 ng.kg body wt-1.h-1) into the lateral cerebral ventricle of freely moving rats caused a dose-dependent increase in the number of central-apneic episodes during rapid-eye-movement sleep without affecting the time spent in rapid-eye-movement sleep or basic respiratory rate. These results suggest that endogenous digitalis-like factors may be involved in the genesis of central sleep apneas.

scholarly journals Induction of interleukin-1 in glia, and its significance in the central nervous system.

1994 ◽  
Vol 64 ◽  
pp. 59
Author(s):  
Yasuko Tomozawa ◽  
Masabumi Minami ◽  
Kazuki Yabuuchi ◽  
Masamichi Satoh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
The Central Nervous System

Effect of a central CRF antagonist on cardiovascular and thermoregulatory responses induced by stress or IL-1 beta

1993 ◽  
Vol 265 (4) ◽  
pp. R834-R839 ◽  
Author(s):  
T. Nakamori ◽  
A. Morimoto ◽  
N. Murakami
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Corticotropin Releasing Factor ◽  
Mild Stress ◽  
Induced Responses ◽  
Interleukin 1 Beta ◽  
The Central Nervous System ◽  
Beta 2

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.

Interleukin-1 and interleukin-6 modify protein phosphorylation in the central nervous system ofHirudo medicinalis

1994 ◽  
Vol 641 (1) ◽  
pp. 155-159 ◽  
Author(s):  
Daniele Bottai ◽  
Mercedes Garcia-Gil ◽  
Maria Luisa Zaccardi ◽  
Loredana Fineschi ◽  
Marcello Brunelli
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Phosphorylation ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
The Central Nervous System ◽  
Modify Protein

Intracerebroventricular infusion of RU28318 blocks aldosterone-salt hypertension

1990 ◽  
Vol 258 (3) ◽  
pp. E482-E484 ◽  
Author(s):  
E. P. Gomez-Sanchez ◽  
C. M. Fort ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Systolic Blood Pressure ◽  
Urine Volume ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Salt Hypertension ◽  
The Central Nervous System ◽  
Dose Dependent

The chronic intracerebroventricular (icv) infusion of aldosterone in rats and dogs elevates the blood pressure within 10-14 days at doses far below those that produce hypertension systemically. The effect in rats is dose dependent and blocked by the concomitant icv infusion of the antimineralocorticoid, prorenone. The effect of the icv infusion of RU28318, another specific spironolactone mineralocorticoid antagonist, on the hypertension produced by chronic subcutaneous (sc) administration of aldosterone in sensitized rats was reported. Miniosmotic pumps were used to deliver 1 micrograms/h aldosterone sc and 1.1 micrograms/h RU8318 icv. Over a 24-day period the indirect systolic blood pressure of the control, RU28318 icv, and aldosterone sc plus RU28318 icv groups increased from 105 to 123 mmHg and were not significantly different from each other, whereas the aldosterone sc group increased to 156 mmHg. RU28318, icv or sc, did not alter the increase in urine volume produced by aldosterone sc, and there was no significant differences in weight between the groups. This study provides evidence of the importance of the central nervous system in the pathogenesis of hypertension produced by systemic mineralocorticoid excess.

Interleukin-1: A cytokine that has potent antisecretory and anti-ulcer actions via the central nervous system

1990 ◽  
Vol 173 (2) ◽  
pp. 585-590 ◽  
Author(s):  
Akira Uehara ◽  
Toshikatsu Okumura ◽  
Shigeru Kitamori ◽  
Yuichi Takasugi ◽  
Masayoshi Namiki
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
The Central Nervous System

Reserpine-induced central effects: pharmacological evidence for the lack of central effects of reserpine methiodide

2005 ◽  
Vol 83 (6) ◽  
pp. 509-515 ◽  
Author(s):  
Srinivas Nammi ◽  
Krishna Murthy Boini ◽  
Sushruta Koppula ◽  
Satyanarayana Sreemantula
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Target Tissue ◽  
Central Effects ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
Rats And Mice ◽  
Dose Dependent ◽  
Higher Doses

Reserpine, an alkaloid from Rauwolfia serpentina, was widely used for its antihypertensive action. However, its use has been reduced because of its sedative and extra pyramidal symptoms. In the present investigation, reserpine methiodide (RMI), a quaternary analogue of reserpine, was synthesized and pharmacologically evaluated in rats and mice for its central (barbiturate hypnosis, spontaneous motor activity, body temperature, and avoidance of conditioned response) and peripheral actions (blood pressure) in comparison with reserpine. The results indicate that reserpine produced a dose-dependent depression of the central nervous system. RMI at doses equal to and double the equimolar doses of reserpine did not produce any behavioural changes compared with control animals. Nevertheless, both reserpine and RMI were found to produce dose-dependent reduction in the blood pressure of anaesthetized rats, although only at higher doses of RMI, indicating that quaternization of reserpine not only attenuated the entry of RMI into the central nervous system, but also reduced its access to the target tissue in the periphery. It is speculated that the hypotensive actions of RMI may also be due to peripheral depletion of catecholamines. Key words: resperine methiodide (RMI), reserpine, behaviour, blood pressure, mice, rats.

scholarly journals Inflammatory Cytokine Profile and Plasticity of Brain and Spinal Microglia in Response to ATP and Glutamate

2021 ◽  
Vol 15 ◽  
Author(s):  
Sam Joshva Baskar Jesudasan ◽  
Somnath J. Gupta ◽  
Matthew A. Churchward ◽  
Kathryn G. Todd ◽  
Ian R. Winship
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Surrounding Environment ◽  
Glial Cultures ◽  
Inflammatory Phenotype ◽  
The Central Nervous System ◽  
Molecular Patterns

Microglia are the primary cells in the central nervous system that identify and respond to injury or damage. Such a perturbation in the nervous system induces the release of molecules including ATP and glutamate that act as damage-associated molecular patterns (DAMPs). DAMPs are detected by microglia, which then regulate the inflammatory response in a manner sensitive to their surrounding environment. The available data indicates that ATP and glutamate can induce the release of pro inflammatory factors TNF (tumor necrosis factor), IL-1β (interleukin 1 beta), and NO (nitric oxide) from microglia. However, non-physiological concentrations of ATP and glutamate were often used to derive these insights. Here, we have compared the response of spinal cord microglia (SM) relative to brain microglia (BM) using physiologically relevant concentrations of glutamate and ATP that mimic injured conditions in the central nervous system. The data show that ATP and glutamate are not significant modulators of the release of cytokines from either BM or SM. Consistent with previous studies, spinal microglia exhibited a general trend toward reduced release of inflammatory cytokines relative to brain-derived microglia. Moreover, we demonstrate that the responses of microglia to these DAMPs can be altered by modifying the biochemical milieu in their surrounding environment. Preconditioning brain derived microglia with media from spinal cord derived mixed glial cultures shifted their release of IL-1ß and IL-6 to a less inflammatory phenotype consistent with spinal microglia.

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