Desflurane reduces the febrile response to administration of interleukin-2

BACKGROUND: Intraoperative fever is relatively rare considering how often pyrogenic causes are likely to be present and how common fever is postoperatively. This low incidence suggests that general anesthesia per se inhibits the normal response to pyrogenic stimulation. The authors therefore tested the hypothesis that desflurane-induced anesthesia produces a dose-dependent inhibition of the febrile response. METHODS: Eight volunteers were studied, each on 3 study days. Each was given an intravenous injection of 50,000 IU/ kg of interleukin-2 (elapsed time, 0 h), followed 2 h later by 100,000 IU/kg. One hour after the second dose, the volunteers were assigned randomly to three doses of desflurane to induce anesthesia: (1) 0.0 minimum alveolar concentration (MAC; control), (2) 0.6 MAC, and (3) 1.0 MAC. Anesthesia continued for 5 h. Core temperatures were recorded from the tympanic membrane. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients; shivering was evaluated with electromyography. Integrated and peak temperatures during anesthesia were compared with repeated-measures analysis of variance and Scheffé's F tests. RESULTS: Values are presented as mean +/- SD. Desflurane reduced the integrated (area under the curve) febrile response to pyrogen, from 7.7 +/- 2.0 degrees C x h on the control day to 2.1 +/- 2.3 degrees C x h during 0.6 MAC and to -1.4 +/- 3.1 degrees C x h during 1.0 MAC desflurane-induced anesthesia. Peak core temperature (elapsed time, 5-8 h) decreased in a dose-dependent fashion: 38.6 +/- 0.5 degrees C on the control day, 37.7 +/- 0.7 degrees C during 0.6 MAC and 37.2 +/- 1.0 degrees C during 1.0 MAC desflurane anesthesia. Rising core temperature was always associated with fingertip vasoconstriction and often with shivering. CONCLUSIONS: Desflurane-induced anesthesia produced a dose-dependent decrease in integrated and peak core temperatures after administration of pyrogen, with 1.0 MAC essentially obliterating fever. Anesthetic-induced inhibition of the pyrogenic response is therefore one reason that fever is an inconsistent clinical response to inflammation during surgery.     

Hatching of common carp (Cyprinus carpio L.) embryos stored at 4 and -2 degrees C in different concentrations of methanol and sucrose

The hatching performance of common carp (Cyprinus carpio L.) embryos was examined after 12-72-h storage at 4 and -2 degrees C using different concentrations of sucrose (0.1, 0.25, 0.5 and 1.0 M or 3.42, 8.55, 17.10 and 34.2%), methanol (MeOH) (0.5, 1.0, 1.5, 2.0, 2.5, 3.0 and 3.5 M or 1.6, 3.2, 4.8, 6.4, 8.0, 9.6 and 11.2%), or varying concentrations of methanol in 0.5 M (17.10%) sucrose. For sucrose, 0.5 M (17.10%) showed the maximum survival (41+/-1% (12 h) to 11+/-1.5% (72 h)) at 4 degrees C. No survival was observed at -2 degrees C with any concentration of sucrose. At both temperatures employed, hatching was higher with mixed combination of methanol (1.5 M or 4.8%) and 0.5 M (17.10%) sucrose (4 degrees C: 41+/-1.5% (12 h), 38+/-1.2% (72 h); -2 degrees C: 33+/-1.7% (12 h), 28+/-1.2% (72 h)) compared to methanol alone (4 degrees C: 38+/-1.5% (12 h), 35+/-2.5% (72 h); -2 degrees C: 31+/-2.5% (12 h), 25+/-2% (72 h)). The combination of 1.5 M (4.8%) methanol and 0.5 M (17.10%) sucrose produced the best results among all the concentrations tested at both temperatures.     

A correlation between membrane fluidity and the critical temperature for cell adhesion

BHK 21 cells can adhere to a protein-coated plastic dish in the presence of Ca2+ at temperatures above 12 degrees C. However, they cannot adhere below 8 degrees C. The ESR spectrum of cells spin-labeled with a stearic acid label indicated that the membrane fluidity changed characteristically at 10 degrees C, 20 degrees C, and 30 degrees C. The critical temperature for cell adhesion coincided well with one of the characteristic temperatures for the membrane fluidity change. In the case of adhesion in the presence of Mg2+, no such correlation was observed.     

Selective convective brain cooling during normothermic cardiopulmonary bypass in dogs

BACKGROUND: Neurologic complications, primarily resulting from ischemic insults, represent the leading cause of morbidity and disability, and the second most common source of death, after cardiac operations. Previous studies have reported that increases (as occur during the rewarming phase of cardiopulmonary bypass [CPB]) or decreases in brain temperature of a mere 0.5 degrees to 2 degrees C can significantly worsen or improve, respectively, postischemic neurologic outcome. The purpose of the present study was to evaluate a novel approach of selectively cooling the brain during hypothermic CPB and subsequent rewarming. METHODS: Sixteen dogs were anesthetized with either intravenous pentobarbital or inhaled halothane (n = 8 per group). Normocapnia (alpha stat technique) and a blood pressure near 75 mm Hg were maintained. Temperatures were monitored by placing thermistors in the esophagus (i.e., core), parietal epidural space, and brain parenchyma at depths of 1 and 2 cm beneath the dura. During CPB, core temperature was actively cycled from 38 degrees C to 28 degrees C, and then returned to 38 degrees C. Forced air pericranial cooling (air temperature of approximately 13 degrees C) was initiated simultaneous with the onset of CPB, and maintained throughout the bypass period. Brain-to-core temperature gradients were calculated by subtracting the core temperature from regional brain temperatures. RESULTS: In halothane-anesthetized dogs, brain temperatures at all monitoring sites were significantly less than core during all phases of CPB, with one exception (2 cm during systemic cooling). Brain cooling was most prominent during and after systemic rewarming. For example, during systemic rewarming, average temperatures in the parietal epidural space, and 1 and 2 cm beneath the dura, were 3.3 degrees +/- 1.3 degrees C (mean +/- standard deviation), 3.2+/-1.4 degrees C, and 1.6 degrees +/-1.0 degrees C, cooler than the core, respectively. Similar trends, but of a greater magnitude, were noted in pentobarbital-anesthetized dogs. For example, during systemic rewarming, corresponding brain temperatures were 6.5 degrees +/-1.7 degrees C, 6.3 degrees +/-1.6 degrees C, and 4.2+/-1.3 degrees C cooler than the core, respectively. CONCLUSIONS: The magnitude of selective brain cooling observed in both study groups typically exceeded the 0.5 degrees to 2.0 degrees C change previously reported to modulate ischemic injury, and was most prominent during the latter phases of CPB. When compared with previous research from our laboratory, application of cold forced air to the cranial surface resulted in brain temperatures that were cooler than those observed during hypothermic CPB without pericranial cooling. On the basis of the assumption that similar beneficial brain temperature changes can be induced in humans, we speculate that selective convective brain cooling may enable clinicians to improve neurologic outcome after hypothermic CPB.     

Elevated environmental temperatures can induce hyperthermia during d-fenfluramine exposure and enhance 5-hydroxytryptamine (5-HT) depletion in the brain

d-Fenfluramine (d-Fen) has been demonstrated to alter body temperature (BT), decrease 5-hydroxytryptamine (5-HT) and decrease 5-HT plasma membrane transporters (PMT) in rats. Therefore, experiments were designed to test whether a correlation existed between elevated BT and brain 5-HT depletions. It was hypothesized that d-Fen would induce hyperthermia if the environmental temperature was elevated. Experiments were conducted to determine 1) the dose-response of d-Fen on BT in a 28 degrees C environment, 2) the acute effect of d-Fen on long-term depletion of 5-HT and 5-HT PMT in a 4 degrees C, 22 degrees C or 28 degrees C environment and 3) the effect of a 22 degrees C environment vs. a 28 degrees C environment on the plasma levels of d-Fen and d-norfenfluramine. d-Fen produced a dose-dependent elevation of BT in the 28 degrees C environment, decreased BT in the 4 degrees C environment and had no effect on BT in the 22 degrees C environment. Exposure to d-Fen in the 4 degrees C or 22 degrees C environment reduced 5-HT and 5-HT PMT concentrations compared with control. However, greater reductions of 5-HT and 5-HT PMT concentrations occurred in the 28 degrees C environment. Conversely, the plasma levels of d-Fen and d-norfenfluramine were not altered. Thus these experiments demonstrate that increased BT during d-Fen exposure occurs at elevated environmental temperatures without altering the plasma concentrations of the drug and results in an enhanced long-term depletion of brain 5-HT and 5-HT PMT.     

Postanesthetic vasoconstriction slows peripheral-to-core transfer of cutaneous heat, thereby isolating the core thermal compartment

Forced-air warming during anesthesia increases core temperature comparably with and without thermoregulatory vasoconstriction. In contrast, postoperative forced-air warming may be no more effective than passive insulation. Nonthermoregulatory anesthesia-induced vasodilation may thus influence heat transfer. We compared postanesthetic core rewarming rates in volunteers given cotton blankets or forced air. Additionally, we compared increases in peripheral and core heat contents in the postanesthetic period with data previously acquired during anesthesia to determine how much vasomotion alters intercompartmental heat transfer. Six men were anesthetized and cooled passively until their core temperatures reached 34 degrees C. Anesthesia was then discontinued, and shivering was prevented by giving meperidine. On one day, the volunteers were covered with warmed blankets for 2 h; on the other, volunteers were warmed with forced air. Peripheral tissue heat contents were determined from intramuscular and skin thermocouples. Predicted changes in core temperature were calculated assuming that increases in body heat content were evenly distributed. Predicted changes were thus those that would be expected if vasomotor activity did not impair peripheral-to-core transfer of applied heat. These results were compared with those obtained previously in a similar study of anesthetized volunteers. Body heat content increased 159 +/- 35 kcal (mean +/- SD) more during forced-air than during blanket warming (P < 0.001). Both peripheral and core temperatures increased significantly faster during active warming: 3.3 +/- 0.7 degrees C and 1.1 +/- 0.4 degrees C, respectively. Nonetheless, predicted core temperature increase during forced-air warming exceeded the actual temperature increase by 0.8 +/- 0.3 degree C (P < 0.001). Vasoconstriction thus isolated core tissues from heat applied to the periphery, with the result that core heat content increased 32 +/- 12 kcal less than expected after 2 h of forced-air warming (P < 0.001). In contrast, predicted and actual core temperatures differed only slightly in the anesthetized volunteers previously studied. In contrast to four previous studies, our results indicate that forced-air warming increases core temperature faster than warm blankets. Postanesthetic vasoconstriction nonetheless impeded peripheral-to-core heat transfer, with the result that core temperatures in the two groups differed less than might be expected based on systemic heat balance estimates. Implications: Comparing intercompartmental heat flow in our previous and current studies suggests that anesthetic-induced vasodilation influences intercompartmental heat transfer and distribution of body heat more than thermoregulatory shunt vasomotion.     

Agreement between rectal and tympanic membrane temperatures in marathon runners

STUDY OBJECTIVE: To determine the agreement between rectal temperature and infrared tympanic membrane temperatures in marathon runners presenting to a field hospital at the finish line. METHODS: The subjects of this prospective, blinded, controlled study were runners 18 years or older who were triaged to the acute care medical area at the finish line for suspected hypothermia, hyperthermia, dehydration, or altered mental status. Rectal and tympanic temperatures were measured simultaneously in all subjects for whom rectal temperature measurement had been deemed necessary and recorded on separate data cards. RESULTS: Of the 239 runners treated in the acute care medical area, 37 required rectal temperature measurement and were enrolled in the study. The mean rectal temperature was 38.45 degrees +/- 1.20 degrees C (range, 35.9 degrees to 41.5 degrees C). The mean tympanic membrane temperature was 37.81 degrees +/- 95 degrees C (range, 36.3 degrees to 40.4 degrees C). Pearson's correlation coefficient revealed a moderate correlation (r = .6902, P = .00023). The mean temperature difference between the two thermometers, mean rectal minus mean tympanic membrane, was .64 degrees C (95% confidence interval, .35 degrees to .93 degrees C). Sixty-Two percent of the tympanic membrane readings were within 1 degree C of their rectal counterparts. Agreement ranged from 1.16 degrees (+2 SD) to -2.95 degrees (-2 SD). The 95% confidence interval was 1.67 degrees to -2.95 degrees C. CONCLUSION: We were able to demonstrate only a moderate correlation between the two thermometer readings, with a wide spread between the limits of agreement. This spread could be clinically significant and therefore limits the usefulness of tympanic temperature in the marathon race setting. Because of the potentially large and clinically significant differences in rectal and tympanic temperatures and the limitations inherent in our study, we cannot endorse the use of tympanic temperature in the setting of a marathon event.     

Mild posttraumatic hypothermia reduces mortality after severe controlled cortical impact in rats

The effect of posttraumatic hypothermia (brain temperature controlled at 32 degrees C for 4 h) on mortality after severe controlled cortical impact (CCI) was studied in rats. Four posttraumatic brain temperatures were compared: 37 degrees C (n = 10), 36 degrees C (n = 4), 32 degrees C (n = 10), and uncontrolled (UC; n = 6). Rats were anesthetized and subjected to severe CCI (4.0-m/s velocity, 3.0-mm depth) to the exposed left parietal cortex. At 10 min posttrauma the rats were cooled or maintained at their target brain temperature, using external cooling or warming. Brain temperature in the UC group was recorded but not regulated, and rectal temperature was maintained at 37 +/- 0.5 degrees C. After 4 h, rats were rewarmed over a 1-h period to 37 degrees C, extubated, and observed for 24 h. In the 37 and 36 degree C groups, 24-h mortality was 50% (37 degrees C = 5/10, 36 degrees C = 2/4). In the 32 degree C group, 24-h mortality was 10% (1/10). In the UC group, brain temperature was 35.4 +/- 0.6 degrees C during the 4-h treatment period and 24-h mortality was 0% (0/6). Mortality was higher in groups with brain temperatures > or = 36 degrees C versus those with brain temperatures < 36 degrees C (50 vs. 6%, respectively; p < 0.05). Additionally, electroencephalograms (EEG) were recorded in subsets of each temperature group and the percentage of time that the EEG was suppressed (isoelectric) was determined. Percentage of EEG suppression was greater in the hypothermic (32 degrees C, n = 6; UC, n = 4) groups than in the normothermic (36 degrees C, n = 3; 37 degrees C, n = 6) groups (23.3 +/- 14.3 vs. 1.2 +/- 3.1%, respectively; p < 0.05). Posttraumatic hypothermia suppressed EEG during treatment and reduced mortality after severe CCI. The threshold for this protective effect appears to be a brain temperature < 36 degrees C. Thus, even mild hypothermia may be beneficial after severe brain trauma.     

Do amoebic liver abscesses start as large lesions? Case report of an evolving amoebic liver abscess

Paired tympanic membrane and rectal temperatures were compared for 103 female fallow deer (Dama dama) after short-term anesthesia to determine if tympanic temperature was a reliable indicator of hyperthermia associated with handling stress. Each deer was restrained in a drop-floor chute, anesthetized by i.v. injection of xylazine hydrochloride and ketamine hydrochloride, and removed from the chute. After a short procedure was completed, i.m. antibiotics and i.v. yohimbine hydrochloride were given to each deer. Temperature measurements were obtained during recovery from anesthesia, approximately 10 min after initial restraint. Mean tympanic temperature (38.6 degrees C +/- 0.7 degrees C; range 37.4-40.8 degrees C) was significantly lower than mean rectal temperature (40.1 degrees C +/- 0.8 degrees C; range 37.5-42.0 degrees C) [corrected]. One animal had rectal and tympanic temperatures of 42.0 degrees C and 40.8 degrees C, respectively, but regained normal body temperature after cooling measures were applied. Tympanic membrane temperature measurement may provide a method for evaluation of body temperature by separating retained body heat caused by exertion from critical elevations in core body temperature associated with clinical disease or capture stress.     

Identification of murine p120 isoforms and heterogeneous expression of p120cas isoforms in human tumor cell lines

Heat stress is a common problem for cattle. General consequences of heat stress include increased body temperatures and reduced feed intakes. As a measure of heat stress, core body temperatures of unshaded feedlot steers (crossbred Bos taurus) were monitored from mid-June to early November in Nebraska using transmitters implanted in the peritoneum of 10 steers (initially 10 mo of age). Steers were fed at 0630 and 1430 using a finishing diet of 1.52 NEg Mcal/kg with 13% protein and 4% roughage per day and housed in two open lots with stocking densities of 15.2 or 19.3 m2/steer. Core body temperatures, ambient temperature, relative humidity, and wind speed were measured at 3-min intervals and mathematically filtered to produce 120 readings/ d. For 94 usable daily records, body temperature means (39.04 +/- .12 degrees C), maxima (39.89 +/- .21 degrees C at 1836 +/- .73 h), minima (38.33 +/- .29 degrees C at 0823 +/- .38 h), and patterns were similar among steers. As daily maximum ambient temperatures increased, minimum body temperatures decreased slightly (.04 degree C per 5 degrees C; P < .01). After daily maximum ambient temperatures reached a threshold of 25.6 degrees C, daily maximum body temperatures increased linearly with maximum ambient temperatures (.42 degree C per 5 degrees C; P < .01). Sharp peaks in body temperature were often seen in the late evening (approximately 2200) after ambient temperature had decreased to well below maximum values. These evening peaks occurred on an average of 25% of the days, had amplitudes ranging from .7 to 3.5 degrees C relative to mean daily temperatures and lasted for 1.5 h. From a practical standpoint, we suggest that producers monitor meteorological forecast of peak ambient temperatures and make special efforts, such as spraying animals, when exceptionally hot weather is predicted.     

Small changes in ambient temperature cause large changes in 3,4-methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat

The amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) is a drug of abuse and has been shown to be neurotoxic to 5-HT terminals in many species. MDMA-engendered neurotoxicity has been shown to be affected by both ambient temperature and core body temperature. We now report that small (2 degreesC) changes in ambient temperature produce changes in core temperature in MDMA-treated rats, but the same changes in ambient temperature do not affect core temperature of saline-treated animals. Furthermore, increases in core temperature of MDMA-treated animals increase neurotoxicity. Rats were given MDMA (20 or 40 mg/kg) or saline and placed in an ambient temperature of 20, 22, 24, 26, 28, or 30 degreesC using a novel temperature measurement apparatus that controls ambient temperature +/-0.5 degrees C. Two weeks after MDMA treatment, the rats were killed, and regional 5-HT and 5-hydroxyindole acetic acid levels were analyzed as a measure of neurotoxicity. Rats treated with MDMA at 20 and 22 degrees C showed a hypothermic core temperature response. Treatment with MDMA at 28 and 30 degreesC produced a hyperthermic response. At ambient temperatures of 20-24 degrees C, neurotoxicity was not observed in the frontal cortex, somatosensory cortex, hippocampus, or striatum. At ambient temperatures of 26-30 degrees C, neurotoxicity was seen and correlated with core temperature in all regions examined. These data indicate that ambient temperature has a significant affect on MDMA neurotoxicity, core temperature, and thermoregulation in rats. This finding has implications on both the temperature dependence of the mechanism of MDMA neurotoxicity and human use because fatal hyperthermia is associated with MDMA use in humans.     

Thermoregulatory effects of caffeine ingestion during submaximal exercise in men

BACKGROUND: The exclusive effect of caffeine ingestion on exercise thermoregulation is unclear; data indicate that caffeine may have a positive effect, a negative effect, or no effect. METHODS: Rectal (TRE) and mean skin (TSK) temperatures, skin heat conductance (HSK), and sweat rate (MSW) were measured during 30 min of rest and subsequent 70 min of submaximal cycle-ergometer exercise (67% VO2PEAK) in 11 aerobically conditioned men (mean +/- SD 29 +/- 6 yr, 49 +/- 6 mL x min(-1) x kg(-1) VO2PEAK) under two conditions: a caffeine (10 mg x kg(-1) ingestion (CI) session and a noncaffeine ingestion (NCI) control session. RESULTS: There were no significant differences in physiological or thermoregulatory parameters during exercise: X (+/-SE) end exercise levels for the NCI and CI sessions, respectively, were VO2 = 2.50 +/- 0.09 vs. 2.55 +/- 0.09 L x min(-1); heart rate = 145 +/- 7 vs. 145 +/- 5 bpm; HSK = 30 +/- 3 vs. 28 +/- 3 kcal x m(-2) x h(-1) x degrees C(-1); MSW = 393 +/- 35 vs. 378 +/- 36 g x m(-2) x h(-1); and TRE = 38.3 +/- 0.2 vs. 38.4 +/- 0.1 degrees C. Control TSK was lower than that for CI by 0.4 to 0.5 degrees C at rest and during exercise. CONCLUSION: Ingestion of a high level (10 mg x kg(-1) of caffeine has no effect on skin heat conductance, sweating, or the rate of increase and final level of rectal temperature during moderate, submaximal leg exercise.     

Effects of topical skin protectant on heat exchange in humans

BACKGROUND: The application of a Topical Skin Protectant (TSP) under chemical protective clothing may impair heat exchange and/or decrease tolerance time during exercise. HYPOTHESIS: The extent to which TSP might act as a barrier to heat transfer was unknown. Since TSP may be permeable to water vapor, we hypothesized that there would be no significant differences between treatments on variables effecting heat exchange. METHODS: There were 10 subjects who walked (3.5 mph, 3% grade) until volitional exhaustion in an environmental chamber (TA = 36.0 +/- 0.5 degrees C; TDP = 27.0 +/- 1.0 degrees C) in two conditions: no TSP application (CON) and TSP application (TSP). TSP was applied to 21% of body surface area on six specific areas. Esophageal temperature, skin temperature (8 sites), heart rate, and pre- and post-experimental weights were measured. Mean skin temperature, mean body temperature, changes in esophageal temperature per min of exercise, evaporative heat loss, and sweating rate were calculated. RESULTS: There was no effect (p < 0.05) of TSP on esophageal temperature, mean skin temperature, heart rate, tolerance time (CON: 139.3 +/- 32.5 vs. TSP: 132.3 +/- 37.0 min), sweating rate (CON: 9.5 +/- 1.9 vs. TSP: 9.4 +/- 3.03 g.min-1) and evaporative heat loss (CON: 200.9 +/- 31.6 vs. TSP: 215.9 +/- 25.9 W.m-2). The change in TES per min of exercise averaged 0.014 +/- 0.003 degree C during TSP and 0.012 +/- 0.003 degree C during CON, and was higher (p = 0.024) in TSP. At this rate, the difference between treatments for 4 h would be 0.48 degree C. There were no adverse local or systemic reactions to TSP application. CONCLUSIONS: TSP application minimally affected heat exchange under the conditions of this study.     

Effects of ambient temperature on the capacity to perform prolonged cycle exercise in man

Eight healthy males performed four rides to exhaustion at approximately 70% of their VO2max obtained in a neutral environment. Subjects cycled at ambient temperatures (Ta) of 3.6 +/- 0.3 (SD), 10.5 +/- 0.5, 20.6 +/- 0.2, and 30.5 +/- 0.2 degrees C with a relative humidity of 70 +/- 2% and an air velocity of approximately 0.7 m.s-1. Weighted mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were recorded at rest, during exercise and at exhaustion. Venous samples were drawn before and during exercise and at exhaustion for determination of hemoglobin, hematocrit, blood metabolites, and serum electrolytes and osmolality. Expired air was collected for calculation of VO2 and R which were used to estimate rates of fuel oxidation. Ratings of perceived exertion (RPE) were also obtained. Time to exhaustion was significantly influenced by Ta (P = 0.001): exercise duration was shortest at 30.5 degrees C (51.6 +/- 3.7 min) and longest at 10.5 degrees C (93.5 +/- 6.2 min). Significant effects of Ta were also observed on VE, VO2, R, estimated fuel oxidation, HR, Tre, Tsk, sweat rate, and RPE. This study demonstrates that there is a clear effect of temperature on exercise capacity which appears to follow an inverted U relationship.     

Malignant melanoma in Europe: changes in mortality rates (1970-90) in European Community countries

We measured metabolic rates (mL O2 h-1, converted to kcal d-1), deep body temperatures (degree C), and skin temperatures (degree C) and calculated whole-animal thermal conductances (mL O2 g-1 h-1 degree C-1) of five 3-yr-old harbor seals (Phoca vitulina concolor) at air temperatures between -20 degrees and 35 degrees C. The mean thermal neutral zone of these seals extended from a lower critical temperature of -12.9 degrees +/- 1.6 degrees C (SD) to an upper critical temperature of 28.6 degrees +/- 1.7 degrees C. Hyperthermia was observed at an ambient air temperature of 35 degrees C. Mean standard metabolic rate was 1,553.6 +/- 168.2 kcal d-1, about 1.2 times the value expected for adult animals of similar body mass (mean mass = 49.2 +/- 7.5 kg). Mean deep body temperature increased from 37.5 degrees +/- 0.30 degrees C at an ambient temperature of 30 degrees C and reached 39.3 degrees +/- 0.33 degrees C at an ambient temperature of 35 degrees C. Skin temperature decreased with decreasing ambient temperature but remained well above ambient temperature. Mean whole-animal thermal conductance decreased from an ambient temperature of 35 degrees C until it reached a minimum value of 0.007 mL O2 g-1 h-1 degree C-1 at -4.0 degrees C; it then increased with a further decrease in ambient temperature. In comparison to the thermal limits of the same seals during their first year of life, the results indicate a broadening of the thermal neutral zone with age: an 11 degrees C decrease in the lower critical temperature and a 3.5 degrees C increase in the upper critical temperature. These findings suggest that warm ambient air temperatures should not pose any particular thermoregulatory problems for larger and older harbor seals, even beyond the limits of their current annual distribution.     

Circadian rhythms of rat internal temperatures and thermal ambiance (author's transl)]

Chronic recording of cerebellar and subcutaneous temperatures were carried out in rats maintained at different ambient temperatures in a 12 h light-dark cycle (light from 7 to 19 h). Cerebellar and subcutaneous temperatures followed a rhythm with a period of 24 h with acrophase at 1 h and an amplitude of 0.75 degrees C. The amplitude and acrophase were not altered by modification of the ambient temperature (20-25-30-34 or 35 degrees C), but each elevation of ambient temperature produced a rise in the mean internal temperature of the rat. This rise, hardly perceptible at ambient temperatures of 25 and 30 degrees C, reaches 0.5 degrees C between 20 and 25 degrees C and 1 degrees C between 30 and 34 degrees C. This elevation of temperature was maintained for the duration of the 10 days of observation. These results pose at least three questions: the degree of liaison between the rhythms of activity (waking) and temperature; the lability of the mean internal temperature, which alter with ambient temperature while the amplitude of the circadian rhythm is unaltered and the absence of reduction of mean interanl temperature several days exposure to a raised ambient temperature, even when activity and metabolism are reduced by the second day of exposure.     

Alfentanil slightly increases the sweating threshold and markedly reduces the vasoconstriction and shivering thresholds

BACKGROUND: Hypothermia is common in surgical patients and victims of major trauma; it also results from environmental exposure and drug abuse. In most cases, hypothermia results largely from drug-induced inhibition of normal thermoregulatory control. Although opioids are given to a variety of patients, the thermoregulatory effects of opioids in humans remain unknown. Accordingly, the hypothesis that opioid administration impairs thermoregulatory control was tested. METHODS: Eight volunteers were studied, each on 3 days: (1) a target total plasma alfentanil concentration of 100 ng/ml, (2) control (no drug), and (3) a target alfentanil concentration of 300 ng/ml. Each day, skin and core temperatures were increased sufficiently to provoke sweating. Temperatures subsequently were reduced to elicit peripheral vasoconstriction and shivering. Mathematical compensations were made for changes in skin temperature using the established linear cutaneous contributions to control of sweating (10%) and to vasoconstriction and shivering (20%). From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C) and unbound plasma alfentanil concentrations, the individual concentration-response relationship was determined. The concentration-response relationship for all the volunteers was determined similarly using total alfentanil concentrations. RESULTS: In terms of unbound concentration, alfentanil increased the sweating threshold (slope = 0.021 +/- 0.016 degrees C.ng-1.ml; r2 = 0.92 +/- 0.06). Alfentanil also significantly decreased the vasoconstriction (slope = -0.075 +/- 0.067 degrees C.ng-1.ml; r2 = 0.92 +/- 0.07) and shivering thresholds (slope = -0.063 +/- -0.037 degrees C.ng-1.ml; r2 = 0.98 +/- 0.04). In terms of total alfentanil concentration (degrees C.ng-1.ml), the sweating threshold increased according to the equation: threshold (degrees C) = 0.0014[alfentanil] + 37.2 (r2 = 0.33). In contrast, alfentanil produced a linear decrease in the core temperature, triggering vasoconstriction: threshold (degrees C) = -0.0049[alfentanil] + 36.7 (r2 = 0.64). Similarly, alfentanil linearly decreased the shivering threshold: threshold (degrees C) = -0.0057[alfentanil] + 35.9 (r2 = 0.70). CONCLUSIONS: The observed pattern of thermoregulatory impairment is similar to that produced by most general anesthetics: a slight increase in the sweating threshold and a substantial, linear decrease in the vasoconstriction and shivering thresholds.     

Energy metabolism and protein balance in growing rats housed in 18 degree C or 28 degree C environments and fed different levels of dietary protein

A study was performed to investigate the effect of environmental temperature and increasing levels of protein in the diet on visceral organ size, digestibility, protein balance and energy metabolism in rats. Thirty-six male Wistar rats, initial body weight 77-80 g, were used in a factorial design consisting of three levels of dietary protein and two environmental temperatures of either 18 or 28 degrees C. Three fish meal-based diets were prepared to contain 91, 171 and 262 g protein (N X 6.25/kg diet). Gas-exchange measurements were made and urine and feces were quantitatively collected. The weights of the visceral organs from rats housed at 18 degrees C were greater (P < 0.05) than those of rats housed at 28 degrees C. The digestibilities of dry matter and protein were not affected by environmental temperature, whereas fat and energy digestibilities were higher (P < 0.05) at 18 degrees C than at 28 degrees C. As the level of protein was increased, the digestibilities of protein, energy and fat increased (P < 0.05). Protein intake and protein retention were higher at 18 degrees C (P < 0.05) than at 28 degrees C and increased (P < 0.05) as dietary protein concentration increased. Apparent biological value was lower (P < 0.05) at 18 degrees C than at 28 degrees C and decreased (P < 0.05) as dietary protein level increased. Heat production as a percentage of metabolizable energy was higher (P < 0.05) for the low protein diet than for the medium and high protein diets. The efficiency of energy utilization was depressed (P < 0.05) for the high protein diet when rats were kept at 28 degrees C. The results suggest that thermogenesis was induced when low protein was fed. The increase in thermogenesis may have been important in regulating energy balance and maintaining a constant body temperature in a cold environment.     

Dexamethasone inhibits the pyrogenic activity of prostaglandin F2 alpha, but not prostaglandin E2

The effect of dexamethasone on prostaglandin (PG) E2- and PGF2 alpha-induced fever was studied in rats. Intracerebroventricular injection of PGE2 and PGF2 alpha (500 ng) induced increases in body temperature (maximal temperature rises of 0.97 +/- 0.13 degrees C and 0.78 +/- 0.18 degrees C, respectively, vs. vehicle 0.12 +/- 0.09 degrees C) of unrestrained rats maintained within the thermoneutral zone. PGE2-induced fever peaked earlier and the defervescence was faster when compared to the response induced by PGF2 alpha. Subcutaneous pre-administration of dexamethasone (0.5 mg/kg) did not affect PGE2-induced fever (maximal temperature rise of 1.00 +/- 0.08 degrees C), but completely prevented the pyrogenic activity of PGF2 alpha (maximal temperature rise of 0.16 +/- 0.16 degrees C). Neither PGE2- nor PGF2 alpha-induced fever was significantly altered (maximal temperature rises of 0.90 +/- 0.11 degrees C and 0.64 +/- 0.14 degrees C, respectively) by intraperitoneal administration of indomethacin (2 mg/kg). These results demonstrate for the first time that glucocorticoids, in addition to inhibiting endotoxin- and cytokine-induced fever, can also modulate the pyrogenic activity of some prostaglandins, possibly via suppression of the synthesis of corticotropin-releasing factor, indicating that multiple mechanisms may be involved in the antipyretic activity of these steroids.     

The ocular blood flow tonograph: a new instrument for the measurement of intraocular pressure in rabbits

OBJECTIVES: To determine the intraprostatic pathologic changes following accurately measured doses of transurethral microwave thermal energy in patients with benign prostatic hyperplasia. METHODS: Eight patients scheduled for prostate surgery were treated for approximately 1 hour without anesthesia using a newly designed microwave treatment catheter that allows a close impedance match to prostate tissue and concentrates thermal energy preferentially in the anterior and lateral prostate gland. Interstitial, urethral, and rectal temperatures were continuously measured using a novel stereotactic thermal mapping technique. Serial sections of prostate tissue harvested during subsequent surgery were evaluated pathologically with prostate mapping. RESULTS: Microwave treatment resulted in marked and continuous intraprostate temperature elevation, while urethral and rectal temperatures remained low. Peak intraprostate temperatures in individual patients reached as high as 80 degrees C. Mean temperature reached a maximum of 54 degrees C at a radial distance of approximately 0.5 cm from the urethra and remained 45 degrees C or higher up to a distance of 1.6 cm. The predominant pathologic findings were uniform hemorrhagic necrosis and tissue devitalization without significant inflammation. The mean distance from the urethra to the viable-necrotic tissue border was 1.6 +/- 0.2 cm (range, 0.5 to 2.5). At this border, no more than 1 mm in thickness, temperature averaged 45.7 +/- 0.6 degrees C, and there was a suggestion that pure stromal nodules were more resistant to thermal injury. CONCLUSIONS: Microwave treatment can destroy obstructive prostate tissue while maintaining innocuous urethral and rectal temperatures. Temperatures of 45 degrees C or higher for approximately 1 hour cause uniform thermoablation of prostate tissue.