Baseline Body Temperature Research Articles

Inverse relationship of baseline body temperature and outcome between ischemic stroke patients treated and not treated with thrombolysis: the Bergen stroke study

High body temperature may promote clot lysis whereas low body temperature is neuroprotective in patients with cerebral infarction. We hypothesized that high body temperature is associated with favorable outcome in patients treated with tissue plasminogen activator (tPA) and that low body temperature is associated with favorable outcome in patients not treated with tPA. Patients (n = 111) who were treated with tPA and patients (n = 139) who were not treated with tPA, but presented within 6 h of stroke onset were included. Patients with no temperature measurements within 6 h of stroke onset were excluded. National Institute of Health Stroke Scale (NIHSS) score was obtained on admission. Modified Rankin score (mRS) was obtained after 1 week. Favorable outcome was defined as mRS 0-2 and unfavorable outcome as mRS 3-6. On logistic regression analysis, high body temperature was independently associated with favorable outcome among patients treated with tPA (OR = 3.7, P = 0.009) and low body temperature was independently associated with favorable prognosis among patients not treated with tPA (OR = 2.0, P = 0.042). Our study suggests that the effect of high body temperature on clot lysis is more important than the neuroprotective effect of low body temperature in the early phase after cerebral infarction treated with tPA.

Effects of opioids and anesthetic drugs on body temperature in cats

ObjectiveTo determine which class of opioid alone or in conjunction with other anesthetic drugs causes post-anesthetic hyperthermia in cats. Study designProspective, randomized, crossover study. AnimalsEight adult, healthy, cats (four spayed females and four castrated males weighing 3.8 ± 0.6 kg). MethodsEach cat was instrumented with a wireless thermistor in the abdominal cavity. Temperature in all phases was recorded every 5 minutes for 5 hours. Population body temperature (PBT) was recorded for ∼8 days. Baseline body temperature is the final 24 hours of the PBT. All injectable drugs were given intramuscularly. The cats were administered drugs in four phases: 1) hydromorphone (H) 0.05, 0.1, or 0.2 mg kg−1; 2) morphine (M) (0.5 mg kg−1), buprenorphine (BUP) (0.02 mg kg−1), or butorphanol (BUT) (0.2 mg kg−1); 3) ketamine (K) (5 mg kg−1) or ketamine (5 mg kg−1) plus hydromorphone (0.1 mg kg−1) (KH); 4) isoflurane in oxygen for 1 hour. Fifteen minutes prior to inhalant anesthetic, cats received either no premed (I), hydromorphone (0.1 mg kg−1) (IH), or hydromorphone (0.1 mg kg−1) plus ketamine (5 mg kg−1) (IHK). ResultsMean PBT for all unmedicated cats was 38.9 ± 0.6 °C (102.0 ± 1 °F). The temperature of cats administered all doses of hydromorphone increased from baseline (p < 0.03) All four opioids (H, M, BUP and BUT) studied increased body temperature compared with baseline (p < 0.005). A significant difference was observed between baseline temperature values and those in treatment KH (p < 0.03). Following recovery from anesthesia, temperature in treatments IH and IHK was different from baseline (p < 0.002). Conclusions and clinical relevanceAll of the opioids tested, alone or in combination with ketamine or isoflurane, caused an increase in body temperature. The increase seen was mild to moderate (<40.1 °C (104.2 °F) and self limiting.

Dorsomedial hypothalamus mediates autonomic, neuroendocrine, and locomotor responses evoked from the medial preoptic area

Previous studies suggest that sympathetic responses evoked from the preoptic area in anesthetized rats require activation of neurons in the dorsomedial hypothalamus. Disinhibition of neurons in the dorsomedial hypothalamus in conscious rats produces physiological and behavioral changes resembling those evoked by microinjection of muscimol, a GABA(A) receptor agonist and neuronal inhibitor, into the medial preoptic area. We tested the hypothesis that all of these effects evoked from the medial preoptic area are mediated through neurons in the dorsomedial hypothalamus by assessing the effect of bilateral microinjection of muscimol into the DMH on these changes. After injection of vehicle into the dorsomedial hypothalamus, injection of muscimol into the medial preoptic area elicited marked increases in heart rate, arterial pressure, body temperature, plasma ACTH, and locomotor activity and also increased c-Fos expression in the hypothalamic paraventricular nucleus, a region known to control the release of ACTH from the adenohypophysis. Prior bilateral microinjection of muscimol into the dorsomedial hypothalamus produced a modest depression of baseline heart rate and body temperature but completely abolished all changes evoked from the medial preoptic area. Microinjection of muscimol just anterior to the dorsomedial hypothalamus had no effect on autonomic and neuroendocrine changes evoked from the medial preoptic area. Thus, activity of neurons in the dorsomedial hypothalamus mediates a diverse array of physiological and behavioral responses elicited from the medial preoptic area, suggesting that the latter region represents an important source of inhibitory tone to key neurons in the dorsomedial hypothalamus.

Attenuation of the influenza virus sickness behavior in mice deficient in Toll-like receptor 3

Certain sickness behaviors occur consistently in influenza-infected humans and mice. These include body temperature changes, somnolence, and anorexia. Several cytokines serve as mediators of the influenza acute phase response (APR), including these sickness behaviors, and one likely inducer of these cytokines is dsRNA produced during viral replication. TLR3 is known to be one of the host cellular components capable of recognizing dsRNA and activating cytokine synthesis. To determine the role of TLR3-detected viral dsRNA in the causation of viral symptoms, TLR3-deficient mice (TLR3 knockouts, or KOs) were infected with a marginally-lethal dose of mouse-adapted X-31 influenza virus. TLR3 KOs and their wild-type (WT) controls were monitored for baseline body temperature, locomotor activity, and sleep profiles prior to infection. Both mouse strains were then infected and monitored for changes in these sickness behaviors plus body weight changes and mortality for up to 14 days post-infection. Consistent with the observations that influenza pathology is reduced in TLR3 KOs, we showed that hypothermia after post-infection day 5 and the total loss of body weight were attenuated in the TLR3 KOs. Sleep changes characteristic of this infection model [particularly increased non-rapid-eye-movement sleep (NREMS)] were also attenuated in TLR3 KOs and returned to baseline values more rapidly. Locomotor activity suppression was similar in both strains. Therefore virus-associated dsRNA detected by TLR3 appears to play a substantial role in mediating several aspects of the influenza syndrome in mice.

The olfactory nerve has a role in the body temperature and brain cytokine responses to influenza virus

Mouse-adapted human influenza virus is detectable in the olfactory bulbs of mice within hours after intranasal challenge and is associated with enhanced local cytokine mRNA and protein levels. To determine whether signals from the olfactory nerve influence the unfolding of the acute phase response (APR), we surgically transected the olfactory nerve in mice prior to influenza infection. We then compared the responses of olfactory-nerve-transected (ONT) mice to those recorded in sham-operated control mice using measurements of body temperature, food intake, body weight, locomotor activity and immunohistochemistry for cytokines and the viral antigen, H1N1. ONT did not change baseline body temperature (Tb); however, the onset of virus-induced hypothermia was delayed for about 13 h in the ONT mice. Locomotor activity, food intake and body weights of the two groups were similar. At 15 h post-challenge fewer viral antigen-immunoreactive (IR) cells were observed in the olfactory bulb (OB) of ONT mice compared to sham controls. The number of tumor necrosis factor α (TNFα)- and interleukin 1β (IL1β)-IR cells in ONT mice was also reduced in the OB and other interconnected regions in the brain compared to sham controls. These results suggest that the olfactory nerve pathway is important for the initial pathogenesis of the influenza-induced APR.

Children with Infantile Neuronal Ceroid Lipofuscinosis Have an Increased Risk of Hypothermia and Bradycardia During Anesthesia

Neuronal ceroid lipofuscinoses (NCLs) are a group of autosomal recessive neurodegenerative diseases characterized by lysosomal accumulation of autofluorescent material in neurons and other cell types. The infantile NCL (INCL) subtype is rare (1 in >100,000 births), the most devastating of childhood subtypes, and is caused by mutations in the gene CLN1, which encodes palmitoyl-protein thioesterase-1. To investigate the incidence of hypothermia and bradycardia during general anesthesia in patients with INCL, we conducted a case-control study to examine the perianesthetic course of patients with INCL and of controls receiving anesthesia for diagnostic studies. Eight children with INCL (mean age 25 mo [range, 10-32] at first anesthetic) and 25 controls (mean age 44 mo [range, 18-92]) underwent 62 anesthetics for nonsurgical procedures. Patients with INCL had neurologic deficits including developmental delay, myoclonus, and visual impairment. Patients with INCL had lower baseline temperature (36.4 +/- 0.1 vs 36.8 +/- 0.1, INCL versus controls, P < 0.007), and during anesthesia, despite active warming techniques, had significantly more hypothermia (18 vs 0 episodes, P < 0.001) and sinus bradycardia (10 vs 1, P < 0.001) compared with controls. INCL diagnosis was significantly associated with temperature decreases during anesthesia (P < 0.001), whereas age, sex, and duration of anesthesia were not (P = NS). We report that patients with INCL have lower baseline body temperature and during general anesthesia, despite rewarming interventions, are at increased risk for hypothermia and bradycardia. This suggests a previously unknown INCL phenotype, impaired thermoregulation. Therefore, when anesthetizing these children, careful monitoring and routine use of warming interventions are warranted.

High-dose paracetamol in stroke: new trials are necessary and feasible

We thank Kasner for his comments on the Paracetamol (Acetaminophen) In Stroke (PAIS) trial.1 Kasner wondered whether the costs and efforts of a second study—aiming to confirm our post-hoc finding of a potential beneficial effect of high-dose paracetamol in patients with a baseline body temperature of 37·0°C to 39·0°C—will counterbalance the alleged small benefit of this treatment. Furthermore, he noted that there is sufficient evidence to prescribe paracetamol in patients with acute stroke and high body temperatures, and, therefore, this approach does not warrant further study.

The effects of measurement site and ambient temperature on body temperature values in healthy older adults: A cross-sectional comparative study

Background Accurate baseline body temperature measurement is essential for assessment. Tympanic membrane temperature (TMT) measurement is popular, but there is no consensus on whether it is as accurate as oral temperature (OT) for use with the elderly at varying ambient temperature levels. Objectives To test agreement between TMT and OT measurement of body temperature among an elderly population; and to explore whether agreement between the two sites depends on ambient temperature. Design A cross-sectional comparison study. Methods Two samples of older community-dwelling adults were recruited from 17 community senior citizen centers in Taipei, Taiwan in winter ( n = 262) and summer ( n = 257) of 2007. TMT and OT were simultaneously measured by electronic infrared ear thermometer and electronic digital thermometer. Ambient temperatures measured by digital thermo-hygrometer of the data collection setting were recorded when body temperature was taken. Results In winter mean TMT was 36.64 °C (S.D. 0.37), and mean OT was 36.74 °C (S.D. 0.18). In summer, the mean TMT was 37.05 °C (S.D. 0.30) and mean OT was 36.85 °C (S.D. 0.22). The relationship between TMT and OT were r = 0.42 ( p < 0.001) in winter and r = 0.57 ( p < 0.001) in summer. The values of OT were used as standard to assess the accuracy of the measurement. The bias between TMT and OT was −0.10 °C (S.D. 0.34) and 95% limits of agreement were 0.57 and −0.77 °C in winter; and bias was 0.20 °C (S.D. 0.25) and 95% limits of agreement were 0.69 and −0.29 °C in summer. The findings of this study demonstrate that the TMT has high variability that may under or over estimate body temperatures. Conclusions There is a lack of agreement in body temperatures values between TMT and OT in community-dwelling elderly in both winter and summer. OT was more stable than TMT regardless of ambient temperature influences. Therefore, the oral cavity is preferable to the TM site for temperature measurement in alert elderly. The limitation of this study is that hospitalized patients who are most likely to need temperature measurement are not included in this study.

The Paracetamol (Acetaminophen) In Stroke (PAIS) trial: a multicentre, randomised, placebo-controlled, phase III trial

High body temperature in the first 12-24 h after stroke onset is associated with poor functional outcome. The Paracetamol (Acetaminophen) In Stroke (PAIS) trial aimed to assess whether early treatment with paracetamol improves functional outcome in patients with acute stroke by reducing body temperature and preventing fever. In a multicentre, randomised, double-blind, placebo-controlled trial, patients with ischaemic stroke or intracerebral haemorrhage and body temperature between 36 degrees C and 39 degrees C were randomly assigned treatment with paracetamol (6 g daily) or placebo within 12 h from symptom onset. Treatment allocation was based on a computer-generated list of random numbers with varying block size. The primary outcome was improvement beyond expectation on the modified Rankin scale at 3 months, according to the sliding dichotomy approach. This trial is registered, number ISRCTN74418480. Between March, 2003, and May, 2008, 1400 patients were randomly allocated treatment. 260 (37%) of 697 patients receiving paracetamol and 232 (33%) of 703 receiving placebo improved beyond expectation (adjusted odds ratio [OR] 1.20, 95% CI 0.96-1.50). In a post-hoc analysis of patients with baseline body temperature 37-39 degrees C, treatment with paracetamol was associated with improved outcome (1.43, 1.02-1.97). There were 55 serious adverse events in the paracetamol group (8%) and 70 in the placebo group (10%). These results do not support routine use of high-dose paracetamol in patients with acute stroke. Paracetamol might have a beneficial effect on functional outcome in patients admitted with a body temperature 37-39 degrees C, but this post-hoc finding needs further study. Netherlands Heart Foundation.

A Full Term Infant with Cyanotic Episodes

A Full Term Infant with Cyanotic Episodes

GABAB(1) Receptor Subunit Isoforms Exert a Differential Influence on Baseline but Not GABAB Receptor Agonist-Induced Changes in Mice

GABA(B) receptor agonists produce hypothermia and motor incoordination. Two GABA(B(1)) receptor subunit isoforms exist, but because of lack of specific molecular or pharmacological tools, the relevance of these isoforms in controlling basal body temperature, locomotor activity, or in vivo responses to GABA(B) receptor agonists has been unknown. Here, we used mice deficient in the GABA(B(1a)) and GABA(B(1b)) subunit isoforms to examine the influence of these isoforms on both baseline motor behavior and body temperature and on the motor-incoordinating and hypothermic responses to the GABA(B) receptor agonists l-baclofen and gamma-hydroxybutyrate (GHB). GABA(B(1b))(-/-) mice were hyperactive in a novel environment and showed slower habituation than either GABA(B(1a))(-/-) or wild-type mice. GABA(B(1b))(-/-) mice were hyperactive throughout the circadian dark phase. Hypothermia in response to l-baclofen (6 and 12 mg/kg) or GHB (1 g/kg), baclofen-induced ataxia as determined on the fixed-speed Rotarod, and GHB-induced hypolocomotion were significantly, but for the most part similarly, attenuated in both GABA(B(1a))(-/-) and GABA(B(1b))(-/-) mice. We conclude that l-baclofen and GHB are nonselective for either GABA(B(1)) receptor isoform in terms of in vivo responses. However, GABA(B(1)) receptor isoforms have distinct and different roles in mediating locomotor behavioral responses to a novel environment. Therefore, GABA(B(1a)) and GABA(B(1b)) isoforms are functionally relevant molecular variants of the GABA(B(1)) receptor subunit, which are differentially involved in specific neurophysiological processes and behaviors.

Sweating It out in a Level III Regional NICU: Disaster Preparation and Lessons Learned at the Ochsner Foundation Hospital

Preparations: In New Orleans, Louisiana, we had been through the drill many times before. Annually, disaster preparation is undertaken in conjunction with our Office of Emergency Preparedness when an imaginary hurricane strikes our city and causes catastrophic damage. Sometimes life imitates art. When Hurricane Katrina crossed the state of Florida and entered the Gulf of Mexico, New Orleans had a metropolitan population of 1.3 million, with 484000 inside the city limits. Much of the city lies slightly below sea level, whereas the level of Lake Pontchartrain typically is 1 foot above sea level. The Alton Ochsner Foundation Hospital is a 531-bed teaching hospital that is situated on the east bank of the Mississippi River, just west of New Orleans in the Parish of Jefferson. Providing incalculable benefit, the first floor of our hospital stands approximately 6 feet above sea level—12 feet above some of the lowest parts of the city of New Orleans. The NICU, located on the 10th floor of this 11-story hospital, was supporting 25 neonates, many of whom were on mechanical ventilation as Katrina approached the Gulf Coast of the United States. One infant was requiring extracorporeal membrane oxygenation (ECMO). The institution had established an emergency-management manual that, although remaining a perpetual work in progress, is currently 122 pages in length and addresses many topics including responses to loss of utilities, external and internal disasters, and severe weather conditions. The Ochsner model of medical care includes many satellite clinics and a closed medical staff for the hospital. Preparing for a natural disaster involves having a facility that would withstand the storm (externally and internally) and having a staff that can care for patients, their families, and all personnel on campus. According to our procedures, after deciding the “essential staff,” “A” and “B” teams are created. The A-team … Address correspondence to Harley G. Ginsberg, MD, FAAP, Neonatal Intensive Care Unit, Alton Ochsner Foundation Hospital, 1514 Jefferson Hwy, New Orleans, LA 70121. E-mail: hginsberg{at}ochsner.org

Body temperature and outcome after stroke thrombolysis

We studied whether baseline body temperature and temperature increases after stroke adversely affect outcome after thrombolysis with intravenous tissue plasminogen activator (IV tPA). The evolution of body temperature in the first 24 h after treatment with IV tPA was described by calculating the area under the curve of the temperature over time plot relative to temperature at admission (AUCBL) and relative to a standard value of 37 degrees C (AUC37). Temperature parameters were related to functional outcome. The median baseline National Institutes of Health Stroke Scale of 100 consecutive patients was 16 (interquartile range 11-21) and 34 patients had a favourable response to tPA. Patients with an unfavourable outcome had a more important temperature elevation than patients who had a favourable outcome after tPA (+1 degrees C vs +0.6 degrees C, P=0.02), despite similar baseline T and had a higher AUCBL (9.79 vs 5.36, P=0.027) and more frequently showed hyperthermia relative to baseline (82% vs 56%, P=0.011). After adjustment for baseline characteristics, the presence of hyperthermia relative to baseline was associated with a reduced odds of good outcome after thrombolysis (OR 0.34, 95% CI 0.10-0.95, P=0.040). Hyperthermia relative to baseline temperature in the 24 h after intravenous thrombolysis is associated with an unfavourable outcome.

Modeling Drug- and System-Related Changes in Body Temperature: Application to Clomethiazole-Induced Hypothermia, Long-Lasting Tolerance Development, and Circadian Rhythm in Rats

The aim of the present investigation was to develop a pharmacokinetic-pharmacodynamic model for the characterization of clomethiazole (CMZ)-induced hypothermia and the rapid development of long-lasting tolerance in rats while taking into account circadian rhythm in baseline and the influence of handling. CMZ-induced hypothermia and tolerance was measured using body temperature telemetry in male Sprague-Dawley rats, which were given s.c. bolus injections of 0, 15, 150, 300, and 600 micromol kg(-1) and 24-h s.c. continuous infusions of 0, 20, and 40 micromol kg(-1) h(-1) using osmotic pumps. The duration of tolerance was studied by repeated injections of 300 micromol kg(-1) at 3- to 32-day intervals. Plasma exposure to CMZ was obtained in satellite groups of catheterized rats. Fitted population concentration-time profiles served as input for the pharmacodynamic analysis. The asymmetric circadian rhythm in baseline body temperature was successfully described by a novel negative feedback model incorporating external light-dark conditions. An empirical function characterized the transient increase in temperature upon handling of the animal. A feedback model for temperature regulation and tolerance development allowed estimation of CMZ potency at 30 +/- 1 microM. The delay in onset of tolerance was estimated via a series of four transit compartments at 7.6 +/- 2 h. The long-lasting tolerance was assumed to be caused by inactivation of a mediator with an estimated turnover time of 46 +/- 3 days. This multicomponent turnover model was able to quantify the CMZ-induced hypothermia, circadian rhythm in baseline, and rapid onset of a long-lasting tolerance to CMZ in rats.

Effect of feed withdrawal and handling intensity on longissimus muscle glycolytic potential and blood measurements in slaughter weight pigs1

This study was carried out to evaluate the effect of feed withdrawal and handling intensity on blood acid-base responses and muscle glycolytic potential in slaughter-weight pigs. Sixty crossbred pigs (BW = 107.7 +/- 0.56 kg; 44 barrows and 16 gilts) were used in a randomized complete block design with a 2 x 2 factorial arrangement of treatments: 1) feed withdrawal (0 vs. 24 h), and 2) handling intensity (low vs. high). The high-intensity handling treatment consisted of moving the pigs through a passage (12.2 m long x 0.91 m wide) for eight laps using an electric goad two times per lap. Pigs in the low-intensity handling treatment were moved at their own pace through the passage for eight laps using a livestock panel and paddle. Biopsy samples were collected from the LM at the beginning of feed withdrawal, at the end of the handling procedure, and 4 h after handling. Blood samples were collected 2 h before and immediately after the handling procedure. There were no interactions between feed withdrawal and handling intensity for any of the variables measured. Feed withdrawal decreased (P < 0.05) baseline and posthandling body temperature (38.85 vs. 38.65 degrees C; SEM = 0.060 and 39.70 vs. 39.37 degrees C; SEM = 0.04, respectively) and blood glucose, lowered (P < 0.05) baseline partial pressure of oxygen and partial pressure of carbon dioxide, and increased (P < 0.01) baseline and posthandling plasma free fatty acid concentrations. High-intensity handling produced higher (P < 0.01) posthandling lactate and glucose, and lower (P < 0.01) posthandling blood pH (7.33 vs. 7.18 +/- 0.02, respectively), bicarbonate, base excess, and total carbon dioxide than low-intensity handling. Longissimus muscle glycolytic potential of fasted pigs was lower (P < 0.01) than in fed pigs at the end of the handling procedure (177.2 vs. 137.0 micromol/g of wet tissue; SEM = 10.08, respectively). There was no effect of handling intensity on longissimus muscle glycolytic potential. Feed withdrawal did not attenuate the blood acid-base changes caused by handling; however, the combination of feed withdrawal and handling decreased muscle glycolytic potential.

Different adaptive traits to cold exposure in young senescence-accelerated mice

A reduced adaptation to cold is a prominent feature in aged mammals, including humans. The accelerated senescence-prone strain of mice (SAMP) has been studied as an animal model for several age-associated disorders and in the acceleration of senescence. Recent studies revealed that SAMP strains have dysfunctional hyperactive mitochondria and are under a higher oxidative stress status from a young age. To investigate whether young SAMP mice show impaired cold adaptation abilities, we performed cold-exposure experiments. There were no strain differences in baseline body temperature and lowest reached temperature during cold exposure. SAMP1 mice took longer times to reach their lowest temperature in comparison to SAMR1 mice. SAMR1 mice showed an elevation in temperature following cold exposure, whereas SAMP1 mice did not. Behavioral observations demonstrated that SAMP1 mice moved more actively than SAMR1 during cold exposure. However, mRNA levels of uncoupling protein 1 (UCP1), a heat generating protein, as well as plasma norepinephrine levels, were higher in SAMP1 than in SAMR1 mice. This newly found physiological phenotype in SAMP1 mice provides us with a tool to clarify the genetic mechanism which accelerates the senescence process and helps us develop medical means which will bring mankind to a healthy old age.

Null mutant analysis of responses to nicotine: deletion of beta2 nicotinic acetylcholine receptor subunit but not alpha7 subunit reduces sensitivity to nicotine-induced locomotor depression and hypothermia.

The nicotinic acetylcholine receptor (nAChR) subtypes alpha4beta2 and alpha7 comprise the majority of brain nicotine-binding sites. Classical genetic strategies using inbred mice and their hybrids suggest that nicotine's effects on locomotor activity and body temperature are influenced by alpha4beta2 but not alpha7 receptors. To evaluate directly the role of these nicotinic subtypes on responses to nicotine, beta2 and alpha7 null mutant (-/-) mice, as well as wild-type (+/+) and heterozygous (+/-) mice, were tested for baseline body temperature and locomotion and nicotine (0-1.5 mg/kg)-induced changes in these responses. Basal responses for these measures were similar for all beta2 genotypes, but baseline Y-maze activity was higher in alpha7-/- mice compared with alpha7+/+ mice. Following nicotine injection, dose-dependent decreases in body temperature and locomotor activity were observed for all three genotypes of both beta2 and alpha7 mice. Although responses in alpha7 mice did not differ among genotypes, beta2 gene deletion was found to have a gene-dependent effect on nicotine's effects. beta2-/- mice were less sensitive to nicotine-induced locomotor depression and hypothermia at low nicotine doses (.25-.5 mg/kg) but were no different from beta2+/+ mice at the highest doses tested (1.0-1.5 mg/kg). Residual responses at high nicotine doses in beta2-/- mice as well as responses in all alpha7 and beta2 mouse genotypes were mediated by nicotinic receptors, since mecamylamine (1.0 mg/kg) blocked all responses following 1.0 mg/kg nicotine. This finding suggests receptors that include the beta2 nAChR subunit partially mediate nicotine's effects on locomotor activity and body temperature.

Isothermic dialysis for hypotension-prone patients.

Standard hemodialysis (dialysate temperature >or=37 degrees C) induces an increase in body temperature capable of eliciting circulatory adjustments dictated by the maintenance of thermal homeostasis. These adjustments oppose, and can overcome, those elicited by the hypovolemia caused by the ultrafiltration process, and thus predispose patients to develop hypotensive crises during the treatment. Hemodynamic studies in hypotension-prone patients treated with standard hemodialysis showed that during the hypotensive crisis the peripheral vascular resistances decrease, while the stroke volume decreases proportionally more than the blood volume, suggesting cardiac underfilling due to blood volume redistribution. On the other hand, removal of the body heat surplus by cool dialysis helped the same patients to sustain their peripheral vasoconstriction and cardiac filling. To prevent the increase in body temperature, dialysate temperature should be regulated in such a way as to remove through the dialyzer the heat surplus accumulated in the body as a result of the ultrafiltration process. The amount of heat removal should be tailored to each patient because there are wide interindividual and intraindividual variations in baseline body temperature and ultrafiltration requirements. This can be accomplished by the use of a device that can adjust the dialysate temperature automatically in order to keep the body temperature of the patient unchanged (isothermic hemodialysis). Isothermic hemodialysis reduced from 50% to 25% the incidence of treatments complicated by episodes of symptomatic hypotension in a large randomized clinical trial involving 95 high-risk patients. The thermoregulated treatment results in better patient tolerance because the cold stress inherent in this procedure is lower than that inflicted by the use of a fixed low temperature as was done in the past. Overall, the available evidence supports the Gotch hypothesis that the increase in body temperature during hemodialysis is due to the ultrafiltration process eliciting peripheral vasoconstriction and heat accumulation in the body. Heat accumulation brings into play the thermal homeostatic mechanisms endangering cardiovascular tolerance to ultrafiltration.

Contrasting Effects of Ibotenate Lesions of the Paraventricular Nucleus and Subparaventricular Zone on Sleep–Wake Cycle and Temperature Regulation

The suprachiasmatic nucleus (SCN), the circadian pacemaker for the brain, provides a massive projection to the subparaventricular zone (SPZ), but the role of the SPZ in circadian processes has received little attention. We examined the effects on circadian rhythms of sleep, body temperature, and activity in rats of restricted ibotenic acid lesions of the ventral or dorsal SPZ that spared the immediately adjacent paraventricular hypothalamic nucleus (PVH) and the SCN. Ventral SPZ lesions caused profound reduction of measures of circadian index of sleep (by 90%) and locomotor activity (75% reduction) but had less effect on body temperature (50% reduction); dorsal SPZ lesions caused greater reduction of circadian index of body temperature (by 70%) but had less effect on circadian index of locomotor activity (45% reduction) or sleep (<5% reduction). The loss of circadian regulation of body temperature or sleep was replaced by a strong ultradian rhythm (period approximately 3 hr). Lesions of the PVH, immediately dorsal to the SPZ, had no significant effect on any circadian rhythms that we measured, nor did the lesions affect the baseline body temperature. However, the fever response after intravenous injection of lipopolysaccharide (5 microg/kg) was markedly decreased in the rats with PVH lesions (66.6%) but not dorsal SPZ lesions. These results indicate that circadian rhythms of sleep and body temperatures are regulated by separate neuronal populations in the SPZ, and different aspects of thermoregulation (circadian rhythm and fever response) are controlled by distinct anatomical substrates.

Lower Baseline Plasma Cortisol and Prolactin together with Increased Body Temperature and Higher mCPP-Induced Cortisol Responses in Men with Pedophilia

There is some evidence that hormonal and serotonergic alterations may play a role in the pathophysiology of paraphilias. The aims of the present study were to examine: 1) baseline plasma cortisol, plasma prolactin, and body temperature; and 2) cortisol, prolactin, body temperature, as well as behavioral responses to meta-chlorophenylpiperazine (mCPP) and placebo in pedophiles and normal men. Pedophiles showed significantly lower baseline plasma cortisol and prolactin concentrations and a higher body temperature than normal volunteers. The mCPP-induced cortisol responses were significantly greater in pedophiles than in normal volunteers. In normal volunteers, mCPP-induced a hyperthermic response, whereas in pedophiles no such response was observed. mCPP induced different behavioral responses in pedophiles than in normal men. In pedophiles, but not in normal men, mCPP increased the sensations “feeling dizzy, ” “restless,” and “strange” and decreased the sensation “feeling hungry”. The results suggest that there are several serotonergic disturbances in pedophiles. It is hypothesized that the results are compatible with a decreased activity of the serotonergic presynaptic neuron and a 5-HT2 postsynaptic receptor hyperresponsivity.