Effects of superior cervical ganglionectomy on body temperature and on the lipopolysaccharide-induced febrile response in rats

2009 ◽  
Vol 209 (1-2) ◽  
pp. 81-86 ◽  
Author(s):  
Horacio E. Romeo ◽  
Delia L. Tio ◽  
Anna N. Taylor
Keyword(s):  
Body Temperature ◽  
Febrile Response ◽  
Superior Cervical Ganglionectomy

scholarly journals Pathophysiology of Fever and Application of Infrared Thermography (IRT) in the Detection of Sick Domestic Animals: Recent Advances

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2316
Author(s):  
Daniel Mota-Rojas ◽  
Dehua Wang ◽  
Cristiane Gonçalves Titto ◽  
Jocelyn Gómez-Prado ◽  
Verónica Carvajal-de la Fuente ◽  
...  
Keyword(s):  
Body Temperature ◽  
Infrared Thermography ◽  
Core Body Temperature ◽  
The Body ◽  
Farm Animals ◽  
Economic Losses ◽  
Febrile Response ◽  
Temperature Range ◽  
Stable Temperature ◽  
Core Body

Body-temperature elevations are multifactorial in origin and classified as hyperthermia as a rise in temperature due to alterations in the thermoregulation mechanism; the body loses the ability to control or regulate body temperature. In contrast, fever is a controlled state, since the body adjusts its stable temperature range to increase body temperature without losing the thermoregulation capacity. Fever refers to an acute phase response that confers a survival benefit on the body, raising core body temperature during infection or systemic inflammation processes to reduce the survival and proliferation of infectious pathogens by altering temperature, restriction of essential nutrients, and the activation of an immune reaction. However, once the infection resolves, the febrile response must be tightly regulated to avoid excessive tissue damage. During fever, neurological, endocrine, immunological, and metabolic changes occur that cause an increase in the stable temperature range, which allows the core body temperature to be considerably increased to stop the invasion of the offending agent and restrict the damage to the organism. There are different metabolic mechanisms of thermoregulation in the febrile response at the central and peripheral levels and cellular events. In response to cold or heat, the brain triggers thermoregulatory responses to coping with changes in body temperature, including autonomic effectors, such as thermogenesis, vasodilation, sweating, and behavioral mechanisms, that trigger flexible, goal-oriented actions, such as seeking heat or cold, nest building, and postural extension. Infrared thermography (IRT) has proven to be a reliable method for the early detection of pathologies affecting animal health and welfare that represent economic losses for farmers. However, the standardization of protocols for IRT use is still needed. Together with the complete understanding of the physiological and behavioral responses involved in the febrile process, it is possible to have timely solutions to serious problem situations. For this reason, the present review aims to analyze the new findings in pathophysiological mechanisms of the febrile process, the heat-loss mechanisms in an animal with fever, thermoregulation, the adverse effects of fever, and recent scientific findings related to different pathologies in farm animals through the use of IRT.

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.

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.

Peptide neurohormones: their role in thermoregulation and fever

1983 ◽  
Vol 61 (7) ◽  
pp. 579-593 ◽  
Author(s):  
W. D. Ruwe ◽  
W. L. Veale ◽  
K. E. Cooper
Keyword(s):  
Body Temperature ◽  
Anterior Commissure ◽  
Extracellular Fluid ◽  
Current Evidence ◽  
Central Administration ◽  
Febrile Response ◽  
Axonal Projections ◽  
The Central Nervous System ◽  
Convulsive Disorders ◽  
The Brain

The neural elements of the rostral diencephalon in the mammal have been implicated in the regulation of body temperature. Moreover, it may be the neural elements within this region of the brain which activate the febrile mechanisms in response to pyrogen. Is it possible that the neuropeptides located within this area of the brain serve as neurochemical intermediaries involved in temperature regulation, fever, and (or) antipyresis? Central administration of several neuropeptides can elicit marked changes in the core temperature of an animal. Although most of these purative neuroregulators exert only a very minor influence on thermoregulation, a small number of the neuropeptides have been shown to have a profound effect on the system controlling this basic vegetative function. One of these peptides, arginine vasopressin (AVP) may play a role as an endogenous antipyretic. The neuroanatomical localization of this peptide, as well as its axonal projections, are consistent with such a role for this neurohypophyseal peptide in the mediation of antipyresis. In addition, current evidence suggests that AVP does function as a neurotransmitter. Examination of the febrile response to pyrogen in both the periparturient animal and the neonate indicates that an elevation in plasma levels of AVP is closely correlated with the diminution in the febrile response. Also, when AVP is perfused into punctate regions of the brain, a pyrogen-induced fever may be markedly suppressed. AVP appears to act primarily within the septal area, 2- to 3-mm rostral to the anterior commissure. During the development of fever, the release of AVP is altered within these same loci. As body temperature decreases during the febrile state, there is a concomitant increase in the amount of AVP released into the extracellular fluid of these septal sites. Very recent findings suggest that AVP may have additional central neurochemical functions. For example, this peptide may be involved in the etiology of some forms of convulsive disorders. The precise manner in which body temperature is regulated by the central nervous system normally and during fever is not well understood. In particular, the central mechanism of action of AVP in these processes remains to be determined. Currently, it is clear that the critical central mechanisms which are active in thermoregulation and fever are quite complex and will require many more years of investigation before the exact role of each can be enunciated.

Temperature responses of lambs after centrally injected prostaglandins and pyrogens

1975 ◽  
Vol 228 (4) ◽  
pp. 1034-1038 ◽  
Author(s):  
QJ Pittman ◽  
WL Veale ◽  
KE Cooper
Keyword(s):  
Body Temperature ◽  
Rectal Temperature ◽  
Lateral Ventricle ◽  
Prostaglandin E1 ◽  
Central Control ◽  
Febrile Response ◽  
Newborn Lamb ◽  
Bacterial Pyrogen ◽  
Temperature Responses

It has been proposed that pyrogens may produce their febrile response by the release of prostaglandins in the hypothalamus. To test this theory, prostaglandin E1 (PGE1) was injected into a lateral ventricle in dosages of 2-200 ug into conscious newborn lambs, ages 4-168 h. Fiifteen of 40 injections were followed by rises in rectal temperature but the remainder were followed either by no change or by falls. Temperature responses did not appear to be related to age and a variation in responses to the same dosage of PGE was often observed. Some lambs were able to develop fevers in response to intravenous bacterial pyrogen yet did not develop fever after intraventricular PGE 1. Intraventricular bacterial pyrogen (3 ng) produced no change in body temperature, whereas three of four injections of 300 ng pyrogen caused fever. The results suggest that the newborn lamb may be able to develop a fever independently of the central involvement of PGE1. Alternatively, the intraventricular approach may not be useful for the study of the central control of body temperature in the newborn lamb.

Kinetics of systemic and intrahypothalamic IL-6 and tumor necrosis factor during endotoxin fever in guinea pigs

1993 ◽  
Vol 265 (3) ◽  
pp. R653-R658 ◽  
Author(s):  
J. Roth ◽  
C. A. Conn ◽  
M. J. Kluger ◽  
E. Zeisberger
Keyword(s):  
Body Temperature ◽  
Tumor Necrosis Factor ◽  
Guinea Pigs ◽  
Tumor Necrosis ◽  
Time Course ◽  
Clear Correlation ◽  
Febrile Response ◽  
Fever Response ◽  
Kinetics Of ◽  
Necrosis Factor

The time course of activity of interleukin-6 (IL-6) and tumor necrosis factor (TNF) was measured in blood plasma and hypothalamic push-pull perfusates during the febrile response to intramuscular injection of bacterial endotoxin (Escherichia coli, 20 micrograms/kg) in 24 guinea pigs. Injection of endotoxin caused a dramatic increase of IL-6 activity in plasma. The logarithmic values of plasma IL-6 activities showed a linear correlation to the febrile change in body temperature (r = 0.898) during the whole time course of fever. IL-6 activity in hypothalamic perfusates increased 12-fold in the first hour after pyrogen application and declined slowly despite the further increase in body temperature. Hypothalamic IL-6 activity did not correlate with the febrile increase in body temperature (r = -0.048). TNF activity in plasma, not detectable before pyrogen application, had its peak in the first hour after endotoxin injection and rapidly declined to 15-20% of the peak activity within the next 2 h and to an undetectable value 5 h after injection. In the hypothalamus TNF was not detectable before endotoxin injection, but it could be monitored in most animals after pyrogen application without a clear correlation to the fever response. These results taken together indicate that endotoxin fever represents a physiological situation in which production and release of cytokines in the peripheral immune system and in the hypothalamus are regulated and stimulated in independent patterns.

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.

Vagal CCK and 5-HT3receptors are unlikely to mediate LPS or IL-1β-induced fever

2000 ◽  
Vol 279 (3) ◽  
pp. R960-R965 ◽  
Author(s):  
S. M. Martin ◽  
B. C. Wilson ◽  
X. Chen ◽  
Y. Takahashi ◽  
P. Poulin ◽  
...  
Keyword(s):  
Body Temperature ◽  
Vagus Nerve ◽  
Adult Male ◽  
Vagal Afferents ◽  
Interleukin 1Β ◽  
Male Rats ◽  
Febrile Response ◽  
Immune Mediators ◽  
Data Support

Previous studies suggested that peripheral immune mediators may involve intermediates acting on the vagus nerve, such as CCK or serotonin (5-HT). We have therefore investigated a possible role for vagal CCK-A and 5-HT3receptors in the febrile response after intraperitoneal human recombinant interleukin-1β (IL-1β) or lipopolysaccharide (LPS). Unanesthetized, adult male rats instrumented with abdominal thermistors were given intraperitoneal CCK-8 sulfate (100 or 150 μg/kg) or 2-methyl-5-hydroxytryptamine maleate (4 mg/kg). In other experiments, rats were treated with either antagonists to the 5-HT3 receptor (ondansetron HCl; 100 μg/kg) or the CCK-A receptor (L-364,718, 100 or 200 μg/kg) in combination with LPS or IL-1β. CCK administration caused a short-lived hypothermia, but interference with the action of endogenous CCK at CCK-A receptors was without effect on IL-1β- or LPS-induced fever. Neither activation of 5-HT3 receptors nor blockade of 5-HT3 receptors affected body temperature or LPS fever. Taken together, our data support the idea that vagal afferents responsive to pyrogenic cytokines may be different from those responsive to CCK or 5-HT.

Biphasic fever: what triggers the second temperature rise?

1995 ◽  
Vol 269 (2) ◽  
pp. R280-R286 ◽  
Author(s):  
A. A. Romanovsky ◽  
C. M. Blatteis
Keyword(s):  
Body Temperature ◽  
Temperature Rise ◽  
Guinea Pigs ◽  
Direct Consequence ◽  
Second Phase ◽  
Febrile Response ◽  
Intravenous Catheters ◽  
Second Peak

The mechanism of initiation of the second body temperature (Tb) rise of the typically biphasic lipopolysaccharide (LPS) fever is not known. This study was undertaken to test the hypothesis that the second Tb rise during fever may be initiated as a direct consequence of the elevated Tb of the first febrile rise. Experiments were conducted in conscious guinea pigs implanted with intraperitoneal thermodes, intravenous catheters, and intrahypothalamic thermocouples. Intraperitoneal cooling (IPC) was performed by perfusing water (22 degrees C) through the thermode under afebrile conditions during the first (0-40 min after pyrogen injection) or second (80-120 min) phase of the biphasic LPS (2 g/kg iv) fever or during a monophasic LPS (0.5 g/kg iv) fever. Throughout IPC, the rate of heat withdrawal was maintained at 11.6 +/- 1.2 mW/g. No IPC was performed in the corresponding controls. When started immediately after LPS administration at the higher dose, IPC completely blocked the first phase of the biphasic fever. This blockade was followed by a Tb rise, which, although similar to the rise in the second phase, might alternatively be interpreted as the delayed occurrence of the first phase previously suppressed by IPC. However, we excluded the later possibility by showing the absence of an overshoot in Tb restoration after IPC applied during the second phase of biphasic fever, during monophasic fever, or under afebrile conditions. We conclude, therefore, that the second Tb rise of biphasic LPS fever is not induced by the elevated Tb of the first febrile phase. The cause of the second peak of the characteristic biphasic febrile response to intravenous LPS remains speculative.

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.

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