Significant Rise In Body Temperature Research Articles

Vital signs changes during different dental procedures: A prospective longitudinal cross-over clinical trial

The purpose of this study was to evaluate the magnitude of vital signs changes during 3 different dental treatments. A prospective longitudinal multiarm cross-over clinical trial was conducted. Three dental procedures were performed on each participant: supragingival scaling, dental restoration under local anesthesia (LA), and exodontia under LA. The following parameters were recorded for in each dental procedure: body temperature (BT), respiratory rate (RR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), and peripheral oxygen saturation (SpO2). Three repeated measurements of each parameter were recorded at 3 phases of each procedure. A total of 150 dental interventions were performed on 50 patients. Scaling caused a statistically significant rise in BT, RR, and SpO2, and a reduction in HR. Restorative treatment caused a statistically significant rise in SpO2 during LA. Exodontia caused a statistically significant rise in BT, RR, SBP (during the procedure), and SpO2 (during LA). Scaling and restorative treatment did not significantly impact heart rate. The respiratory rate may temporarily rise during LA injection and some dental procedures, especially exodontia. Increase in systolic blood pressure and heart rate during exodontia was tolerated by healthy patients.

Febrile Seizure Detect and Alarm System

Wearable medical technology is becoming increasingly popular. Such devices have the potential to vastly improve the effectiveness, safety and economy of monitoring vital signs including temperature by both patients and clinicians. The purpose of this paper is to present design and implementation of a reliable, low cost and non-intrusive system that is to monitor a child’s body temperature using high precision temperature sensor and alarm his/her parents or guardian on their mobile phones as well as on a webpage which can be accessed via internet connection so as to avoid convulsions brought on by a significant rise in body temperature.

Hippocampal Changes in Febrile Infection-Related Epilepsy Syndrome (FIRES)

SummaryBackgroundFebrile seizures are the most common seizure disorder in childhood, associated with a significant rise in body temperature. However, post-infectious refractory afebrile form of seizures in previously healthy children is being increasingly recognized in around the world, which evolves into a chronic refractory form of epilepsy. The term ‘Febrile infection-related epilepsy syndrome’ (FIRES) has been proposed for these conditions and represents a refractory severe post-infectious epileptic condition in previously normal children.Case ReportWe report the initial and follow-up MR imaging findings in a 5year-old with refractory epilepsy post-febrile seizures.ConclusionsIn summary, acute post-infectious seizures are increasingly being recognized across the globe with the newly coined term ‘Febrile infection-related epilepsy syndrome’(FIRES) for this group of immune-mediated epileptic encephalopathy in previously healthy children. This has three phases: episode of simple febrile infection, followed by acute refractory seizures and lastly the chronic phase of neuropsychological impairments and seizures.

Single-trial conditioning in a human taste-endotoxin paradigm induces conditioned odor aversion but not cytokine responses

Immunological responses to bacterial endotoxin can be behaviorally conditioned in rodents. However, it is unclear whether an acute systemic inflammatory response can be behaviorally conditioned in humans. Thus, in a double-blind placebo-controlled study, 20 healthy, male subjects received either a single injection of lipopolysaccharide (LPS) or saline together with a novel tasting beverage (conditioned stimulus, CS). Five days later, all subjects received a saline injection and were re-exposed to the CS. Blood was drawn prior to as well as 0.5, 1.5, 3, 4, 6, and 24 h after LPS administration or CS re-exposure. Endotoxin administration led to transient increases in plasma concentrations of interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α and to a significant rise in body temperature. Sole presentation of the CS during evocation did induce neither alterations in body temperature nor changes in plasma cytokine levels. However, subjects in the experimental group rated the smell of the CS significantly more aversive compared to the control group. Employing endotoxin as a US in a single trial taste-immune conditioning paradigm in humans shows a behaviorally conditioned smell aversion but no learned alterations in cytokine levels.

Stress-induced hyperthermia in the rat: comparison of classical and novel recording methods

Stress causes a rise in body temperature in laboratory animals (stress-induced hyperthermia). However, the direct effect of common stressors in animal research, i.e. transportation between holding and test rooms or isolation of animals, on body temperature has not been investigated to its full extent. To address this question, it is important to have a reliable and simple monitoring technique, which does not induce stress itself. In the present study, we investigated stress-related changes in body temperature of F344/Hw rats after (1) moving the cage within the holding room, (2) moving the cage from the holding room to another test room and (3) social deprivation (isolation). A combination of two different body temperature recording methods was used to clarify their accuracy and stress-inductive character: rectal temperature recording and peritoneal implanted temperature sensors (Thermochron iButtons).The results demonstrate that (1) different stressors induce a significant rise in body temperature, (2) which is detectable for more than 60 min and (3) it is of importance to standardize temperature recording methods in order to avoid confounding effects of the recording method itself. Furthermore, Thermochron iButtons are more accurate and reliable for body temperature studies than rectal recordings.

Effect of maternally derived antibodies on the clinical signs and immune response in pigs after primary and secondary infection with an influenza H1N1 virus

The aim of this study was to determine the role of maternally derived antibodies (MDA) against an influenza H1N1 virus in the clinical protection of piglets and especially their effect on the development of the active immunity after an infection with a homologous influenza H1N1 virus. Twenty piglets with MDA and 10 piglets without MDA were housed together and inoculated twice with influenza H1N1 virus, at 7 and 15 weeks of age. Nine piglets without MDA were added to these groups at 12 weeks of age to be inoculated at 15 weeks of age only. Clinical signs, body temperature, growth performance, virus excretion, antibody responses, and influenza-specific T-cell response were monitored. It was shown that MDA protect piglets against the clinical consequences of a primary influenza infection, but that this protection is not complete. A short but significant rise in body temperature was observed and growth seemed to be inhibited due to the infection. Piglets with MDA shed virus for a longer period after an infection than piglets without MDA. Piglets with and without MDA were protected against the clinical consequences of a secondary infection. However, both after primary and secondary infection significant differences in immune responses were observed that indicated that pigs with MDA developed a weaker immunity than pigs without MDA. Furthermore, overall growth performances from weaning to slaughter show a trend in favour of pigs without maternal antibodies, compared to pigs with maternal antibodies, mainly caused by a significant better performance in the second half of the finishing period. The results of this study provide us insight in the role of MDA in clinical protection and their influence on active immunity after an influenza virus infection of pigs. Furthermore, it leads us to the discussion about the profitability of massive sow herd vaccinations in an attempt to increase MDA levels in piglets, taking into account the overall performance of these piglets and the possible effects on antigenic drift.

Staphylococcal enterotoxin B induces fever, brain c-Fos expression, and serum corticosterone in rats.

The paraventricular nucleus of the hypothalamus (PVH) occupies a pivotal point within the network of brain nuclei coordinating critical host-defense responses. In mice, T cell-dependent immune stimuli, including the bacterial superantigen staphylococcal enterotoxin B (SEB), can activate the PVH. To determine whether T cell-dependent immune stimuli activate the PVH in rats, we assessed plasma corticosterone (Cort) levels, fever responses, and c-Fos expression in the PVH in animals treated with intraperitoneal injections of SEB. In animals with previously implanted abdominal thermisters, intraperitoneal injection of 1 mg/kg SEB resulted in a significant rise in body temperature, with a latency of 3.5-4 h. In separate animals, intraperitoneal injection of 1 mg/kg SEB resulted in a significant elevation of plasma Cort and induced c-Fos expression in parvocellular neurons within the PVH. These results support the idea that T cell-dependent immune stimuli activate brain pathways mediating host-defense responses such as fever and neuroendocrine changes.

Mixing induces long-term hyperthermia in growing pigs

AbstractThe purpose of this experiment was to determine whether body temperature is a sensitive parameter to measure long-term effects of stress in pigs. Mixing of unacquainted pigs is a severe stressor that has detrimental effects on health, production and welfare. We measured deep body temperature after mixing growing pigs. Five pigs of 15 weeks of age, each individually housed with a companion pig, were mixed with two unacquainted congeners. Deep body temperature, heart rate and activity were recorded by radiotelemetry 9 days prior to until 8 days after mixing. These parameters were also recorded in five control pigs (individually housed with a companion pig) during the same time span. Behaviour during the light period was recorded on videotape on the day of mixing and on three subsequent days. Mixing induced a significant rise in body temperature that lasted for 8 h after mixing. Although heart rate and general activity level did not significantly differ between mixed and control pigs, mixing significantly increased the frequency of fighting and reduced the frequency of eating. In conclusion, the present experiment shows that mixing induces a long-lasting hyperthermia in pigs. Thus, deep body temperature may be used as a sensitive parameter to measure long-term effects of stress in pigs.

Neuroprotective effects of human recombinant interleukin-1 receptor antagonist in focal cerebral ischaemia in the rat.

Recombinant human interleukin-1 receptor antagonist (rhIL-1ra) markedly protects against focal cerebral ischaemia in the rat, implicating endogenous IL-1 in the events leading to cerebral infarction. The present experiments investigated the effect of intracerebroventricular (i.c.v.) administration of IL-1 beta or rhIL-1ra on ischaemia damage and physiological parameters after permanent middle cerebral artery occlusion in the rat. IL-1 beta (5 ng. i.c.v.) markedly (92%) enhanced infarct volume and caused a significant rise in body temperature, but rhIL-1ra (10 micrograms, i.c.v.) significantly reduced infarct volume and did not significantly affect heart rate, blood pressure, or body temperature, rhIL-1ra administered 30 min before, or at the time of ischaemia significantly reduced infarct volume in cortex (55 and 60%, respectively) and striatum (52 and 41%, respectively). rhIL-1ra administered 30 min after ischaemia significantly reduced total and cortical infarct volume (26 and 29%, respectively), but did not significantly protect striatal tissue. The effects of rhIL-1ra were still evident in both cortex and striatum 7 days after ischaemia. These results support the role of IL-1 in ischaemic brain damage, revealing potent, sustained, neuroprotective effects of rhIL-1ra in the cortex and striatum, which cannot be attributed directly to changes in physiological parameters.

Obesity, Diet and Body Temperature

Studies conducted thus far on the pathogenesis of obesity have not clearly determined the role of body temperature in the energy balance. In an attempt to explore this relationship further, research has been undertaken, a part of which is represented by the present investigation carried out on 22 adult males: 11 having a BMI less than or equal to 25 (group A) and 11 with BMI greater than 25 (group B). Body temperature was measured by mouth and on the skin surface (in 4 points according to Ramanathan) on 2 consecutive days (every 30 min from noon to 6:30 p.m.), the 1st day with the participants fasting and the 2nd day after consumption of a meal whose energy content represented a part (45%) of the 24-hour energy intake of the subjects, as previously ascertained by a survey of their food consumption. The study was carried out under frequently checked microclimatic conditions. During the week prior to the measurements, the alimentary consumption of the subjects was monitored by direct weighing for 5 consecutive days. A significant rise in body temperature, probably due to dietary thermogenesis, was observed in group A (internal temperature: F = 13.05; skin temperature: F = 6.48) as well as in group B (internal temperature: F = 24.88; skin temperature: F = 5.35) after the meal. However in group B the skin temperature showed a smaller increase than in group A (delta t degree 0.31 vs. 0.49) and an earlier trend towards the basal values (nearly 5 vs. 6 h after the meal). In both groups a decrease in the skin delta t degrees is evident at 3 and 3.5 h, respectively, after the meal, followed by a more remarkable increase in this difference between the 4th and the 5th hour. The meaning of this decrease as well as the difference in body temperature versus caloric intake is discussed. Normal weight individuals demonstrated a positive correlation (r = 0.83) between usual caloric intake per square meter of body surface and fasting internal body temperature. This correlation was not observed in subjects with BMI greater than 25.

Vasopressin and oxytocin in rat brain in response to prostaglandin fever

Urethan-anesthetized rats were used to identify effective stimuli for the release of the peptides arginine vasopressin (AVP) and oxytocin into the ventral septal area (VSA) of the brain. Febrile responses to intracerebroventricular injection of prostaglandin E1 (PGE1) were observed in rats whose body temperatures were maintained at 35, 37, or 39 degrees C. Microinjection of the AVP antagonist d(CH2)5Tyr(Me)AVP into the VSA enhanced fever only when PGE1 administration was associated with a significant rise in body temperature. Passive elevation ("artificial fever") or reduction of body temperature in the absence of a PGE1 stimulus was not affected by the antagonist. Push-pull perfusion of the VSA and the dorsal hippocampus, followed by radioimmunoassay of perfusates for AVP and oxytocin, revealed enhanced release into the VSA of AVP only when PGE1 administration was followed by a rise in body temperature. Oxytocin was released whenever body temperature was raised. Peptide concentrations in simultaneous perfusates of dorsal hippocampus did not change in response to PGE1 administration or to passive elevation of body temperature. We conclude that AVP is released into the VSA, but not the dorsal hippocampus, of the rat during a fever induced by PGE1. Oxytocin is released into the VSA, but not the hippocampus, when temperature is elevated.

Thermal responses to central angiotensin II, SQ 20881, and dopamine infusions in sheep

The thermoregulatory role of brain angiotensin II (ANG II) was tested by intracerebroventricular (IVT) infusion of ANG II or the converting enzyme inhibitor SQ 20881 (SQ) in 15 conscious sheep. Deep body temperature decreased 0.30 +/- 0.07 degree C (SE) during the 3-h period of IVT ANG II (25 ng/min) infusion (P less than 0.05) and increased 0.50 +/- 0.13 degree C during IVT SQ (1 microgram/min) infusion (P less than 0.01). To determine whether the rise in body temperature after IVT SQ infusion might be the result of a central renin-angiotensin system (RAS), SQ was infused IVT in five conscious sheep 20 h after bilateral nephrectomy. This resulted in a significant rise in body temperature of 0.28 +/- 0.05 degree C (P less than 0.05). When vasopressin antidiuretic hormone (ADH) was infused intravenously at the same time of IVT SQ infusion, the rise in temperature was depressed, but ADH did not lower the temperature below basal. IVT dopamine (20 micrograms/min) increased body temperature by 0.40 +/- 0.04 degree C (P less than 0.01), which was qualitatively similar to the result with IVT SQ. These data support the hypothesis that endogenous brain ANG II may play a role in thermoregulation. Furthermore, plasma ADH level, regulated in part by brain ANG II, is probably not the mediator of that thermoregulation. The similar effects of IVT dopamine and SQ on body temperature strengthen the hypothesis that dopamine may be involved in the central action of brain ANG II.

Serum 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine concentrations during acute heat load.

To determine the changes in thyroid hormone metabolism during short periods of exposure to heat, 30 euthyroid healthy male volunteers (aged 23--40 yr) were placed in a climatic chamber for 2 h (35 C, 50% relative humidity). The subjects were at complete rest during the first hour and performed light work (40 watts) during the second hour. Blood samples for T4, T3 and rT3 were drawn at 0, 60, and 120 min. Rectal temperature and heart rate were monitored continuously. No significant changes in T4, T3, rT3, rectal temperature, or heart rate were observed after the first hour (basal levels, 8.5 +/- 0.3 microgram/dl, 160 +/- 5 ng/dl, 14.5 +/- 2.5 ng/dl, 37.2 +/- 0.1 C, and 78 +/- 8 beats/min, respectively; mean +/- SEM). During the second hour, a significant rise in body temperature was recorded (38.5 +/- 0.1 C), accompanied by a significant decrease in mean serum T3 concentration and a rise in mean serum rT3 concentration, T4 concentration remained unchanged. Our findings suggest that, parallel to the elevation in body temperature, there is a shift in the conversion of T4 to the noncalorigenic rT3 metabolite rather than to T3.

Acute effects of a monoamine oxidase inhibitor, tranylcypromine, on thermoregulation in the conscious rabbit.

1. The effect of a single injection of the monoamine oxidase inhibitor, tranylcypromine, administered intravenously (20 mg/kg) or into the lateral cerebral ventricle (5-10 mg), on hypothalamic and rectal temperature, has been investigated.2. Intravenous tranylcypromine causes a significant rise in body temperature, which is due, at least in part, to cutaneous vasoconstriction; this vasoconstriction is augmented by sympathectomy. It is concluded that this vasoconstrictor effect is not mediated via the central nervous system.3. Intraventricular tranylcypromine caused a transient but significant fall in core temperature. This is interpreted as being compatible with selective augmentation of hypothalamic levels of 5-hydroxytryptamine.

Factors Modifying Chlorpromazine Hyperthermia in Young Albino Mice

The administration of dextro -tubocurarine immediately before chlorpromazine was ineffective in modifying the temperature responses of the phenothiazine in 10- and 38-day-old mice. Chlorpromazine sulfoxide, a metabolite of chlorpromazine, produced a profound temperature rise in 10-day-old mice. Morphine sulfate, when given to 10-day-old mice, produced a significant rise in body temperature, which was inhibited completely by the previous administration of nalorphine. In contrast, nalorphine was shown to be ineffective in modifying the body temperature elevation caused by chlorpromazine in this age group. Pilocarpine inhibited the thermogenic response of chlorpromazine by approximately 50 per cent. Cocaine, dl -amphetamine, and reserpine, although demonstrating hyperthermic activity in 10-day-old mice, were unable to modify the response of chlorpromazine on the body temperature of 10-day-old mice. Tripelennamine and insulin, which individually were without a temperature response, were also incapable of altering the temperature response elicited by chlorpromazine in 10-day-old mice. Insulin lowered the blood sugar level significantly in 10-day-old mice, a response not affected by chlorpromazine. The administration of iproniazid before chlorpromazine caused a slight augmentation of the hyperthermic response of the latter, while sodium cyanide, lysergic acid diethylamide, and brom-lysergic acid produced a marked inhibition of the hyperthermic activity of chlorpromazine in 10-day-old mice.

Effects of 2,4-Dinitrophenol on Respiration in the Dog

The intravenous administration of 2,4-dinitrophenol (DNP) to unanesthetized or anesthetized dogs produced an increase in arterial pH and decrease in arterial Pco2 which preceded any significant rise in body temperature. Thus the hyperventilation associated with DNP-administration appears not to be solely the result of increased production of CO2. Although DNP in small amounts stimulated respiration via the carotid body, larger doses still produced increased ventilation and pH and decreased Pco2 after denervation of the carotid bodies and bilateral vagotomy, thus demonstrating a stimulatory effect of DNP at some more central site as well. DNP increased the sensitivity of the respiratory center (or its afferent connections) to Pco2 and/or concentration of hydrogen ion. The similarities of respiratory effects of DNP and salicylate are discussed. An unexplained increase in ‘buffer base’ of the blood occurred in association with the respiratory alkalosis induced by DNP.

Effect of aspirin and reserpine on adrenocortical response to piromen in man.

Conclusions1. Intravenous administration of 0.1 γg Piromen/kg body weight to young, normal male and female subjects causes a significant rise in body temperature and plasma hydrocortisone levels. 2. Increased concentration of plasma free 17-OHCS following Piromen administration has been shown to be the result of increased secretion of hydrocortisone. 3. The rise in plasma hydrocortisone distinctly precedes the elevation of body temperature above 37°C. Fever is, therefore, not the cause of the elevated plasma hydrocortisone levels. 4. The increases in plasma hydrocortisone levels, eosinopenia, temperature, and pulse rate caused by Piromen administration are significantly lessened by the concomitant administration of aspirin. 5. Administration of reserpine in a dose of 4 mg/24-hr period caused no hypothermia in normal human subjects. 6. Pyrogenic, eosinopenic, and adrenocortical stimulatory effects of Piromen are not altered by the prior and concomitant administration of reserpine.

Effect of Autolyzed Yeast, Yeast Nucleic Acid and Related Substances on Body-Temperatures of Rats.

SummarySubcutaneous injection of 2 cc of a “15%” yeast autolysate in rats produced a significant rise in body-temperature. Intraperitoneal injection of the same material produced a significant fall in body-temperature. Both qualitatively and quantitatively similar results were produced by the injection of 2.5 cc of a 0.1% solution of the magnesium salt of yeast nucleic acid. Slight lowering of the body-temperature occurred in some animals after intraperitoneal injection of guanine. Subcutaneous injection of guanine had no effect on body-temperature. Adenine, uracil, xanthine, and allantoin had no effect on the body-temperature of rats by either route of administration.