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Three Gallus domesticus cocks were reared separately in a climatic chamber at 22 degrees C, with lights on at 0600 and off at 1800 h. Food and water were available at all times. At noontime, one bird was handled for the purpose of taking cloacal, comb, and foot temperatures every 3 min for 18 min. Repeated handling produced a fever characterized by a mean rise in core temperature from 41.1 +/- 0.3 degrees C to 41.6 +/- 0.3 degrees C and an initial peripheral vasoconstriction, as shown by a drop in skin temperatures. Maximum core temperature was only 39.9 +/- 0.2 degrees C when the birds received intraperitoneal salicylate 1 h before handling. It is concluded that handling causes a fever in birds. The birds were equipped with an electrocardiogram radio transmitter, and their heart rates were recorded at a distance. When simply touched by an experimenter, the birds' mean heart rate rose from 198 +/- 6 to 249 +/- 15 beats/min. We conclude that fever and tachycardia might indicate the existence of emotion in birds.

Gentle handling of small rodents leads to an emotional fever characterized by a 1-2 degrees C rise in colonic temperature associated with peripheral vasoconstriction and inhibition of this response after administration of salicylate. Because vagotomy has been recently shown to hinder microbial fever, we wanted to know whether emotional fever would also be suppressed by vagotomy in rats. The completeness of subdiaphragmatic vagotomy was verified on the basis of gastric dilation after a 24-h fast. Gentle handling produced fevers of equal magnitude: colonic temperature ca. +1.6 degrees C, in vagotomized and + 1.5 degrees C sham-vagotomized rats. On the other hand, intraperitoneal salicylate (300 mg x kg(-1)) largely prevented the fever response caused by gentle handling. It was concluded that the afferent message in the vagus is not necessary for emotional fever.

Six goldfish, Carassius auratus, weighing 2.5 to 4 g were placed individually in an aquarium with two communicating chambers. One chamber was thermostatted at 34 degrees C, the other at 37 degrees C. In control Session a, without external intervention, fish selected the cooler chamber most of the time and stayed only 4.8 +/- 1.1 min/2 h at 37 degrees C. In Session b, infectious fever was assayed: pyrogen (Salmonella typhosa LPS, or human interleukin-2) was injected intracranially and fish stayed 44.7 +/- 15.3 min/2 h at 37 degrees C. In Session c, behavioral stress was achieved by chasing the fish with a net, catching it, handling it out of water, and injecting 10 microL of saline intracranially. Fish stayed 2.7 +/- 1.0 min/2 h at 37 degrees C. Analysis of variance showed that stay at 37 degrees C was significantly longer in Session b than a and c, and that Sessions a and c were not significantly different from one another. This result confirms the existence of behavioral fever, but does not support the hypothesis of fever in fish after handling.

The problem of the relative hyperpnea occurring at high levels of exercise remains unresolved. This study examined whether the hyperpnea observed in humans during exercise at approximately 70% of maximal work capacity was related to cranial (tympanic) and thoracic (esophageal) temperatures. Six trained male subjects pedaled at approximately 60 revolutions/min on an electrically braked cycle ergometer in a climatic chamber at 25 degrees C and approximately 35% relative humidity in two sessions. The subjects pedaled until exhaustion in two sessions. In one session work rate was increased by 40 W every 2 min and in the other session by 20 W every 2 min. In both exercise sessions, core temperature thresholds for ventilation were evident and subsequently tympanic and esophageal temperatures diverged. This suggested that the hyperpnea in humans observed after approximately 70% of an individual's maximal work rate was determined, in part, by core temperatures and revealed supportive evidence for selective brain cooling in humans.

The present study was conducted to measure nasal mucosal blood flow (NMBF) during body warming. Five subjects [mean (SD) 24 (2) years], wearing only shorts and a thick felt hat with ear flaps, were immersed to the neck in a bath at 40 (0.5) degrees C. Tympanic (Tty), esophageal (Tes), mean unweighted skin (Tsk), nose skin and ear pinna skin were recorded at 1-min intervals. NMBF on the lower septal wall was estimated using a laser Doppler flow meter. At rest Tty and Tes were both 36.5 degrees C. Tty dropped significantly below Tes during body warming, despite impeded heat loss from the head due to the felt hat. Tty increased to 37.3 degrees C and Tes increased to 37.5 degrees C during the immersion. During the immersion all skin temperatures were steady or increasing, ruling out the possibility of a contamination of Tty from Tsk. Body warming significantly (P = 0.001) increased NMBF by approximately three times from resting values at the end of immersion. During the period of increasing core temperatures NMBF was significantly correlated to Tty (r = 0.93, P = 0.0001) and Tes (r = 0.97, P = 0.0001), suggesting the blood flow change in this tissue was a thermoregulatory response. The increased NMBF during hyperthermia supports the hypothesis of respiratory cooling involvement in selective brain cooling of humans.

Humans have higher ventilation when they are hyperthermic but it is not known whether core temperature thresholds for ventilation exist, nor has a physiological rationale been presented for this response. To examine this question, ventilation was studied in relation to core temperatures in humans rendered hyperthermic in a warm bath. Seven subjects [mean (SE), 23.3 (1.4) years] wearing only shorts and a thick felt hat with ear flaps were immersed to the neck in a bath at 41 (0.5) degrees C for 25 min. Tympanic (Tty), esophageal (Tes), thigh skin and forehead skin temperatures, heart rate, inspired minute ventilation (V1 at body temperature and pressure, saturated), ventilation frequency and oxygen consumption (VO2 at standard temperature and pressure, dry) were recorded at 30-s intervals. At immersion V1 briefly increased to 18.6 (3.0) l.min-1, returned to about the pre-immersion value, and significantly increased to 19.3 (3.0) l.min-1 by the end of immersion. VO2 increased significantly from the pre-immersion value of 0.27 l.min-1 to 0.67 l.min-1 by the first 0.5 min of immersion, but then returned to its pre-immersion value. Tty increased to 38.7 (0.2) degrees C and Tes increased to 39.0 (0.2) degrees C by the end of immersion. Core temperature thresholds for increases in V1 were evident at 38.1 degrees C when expressed against Tty and at 38.5 degrees C when expressed against Tes. The results indicated that during body warming core temperature thresholds for V1 are reached and subsequently a hyperpnea was evident, despite VO2 remaining at a resting value.(ABSTRACT TRUNCATED AT 250 WORDS)

A mechanism that selectively cools the brain during hyperthermia is a well-accepted fact in animals. Selective brain cooling (SBC) during hyperthermia has also been proposed in humans, but this suggestion has met with considerable debate. Several authors have rejected the idea of human SBC for the following reasons: 1) SBC is illogical because this mechanism removes the error signal activating the defense against hyperthermia; 2) unlike other animals, humans do not pant and thus do not possess a powerful heat sink at a short distance from the brain; 3) humans do not have a carotid rete, the countercurrent heat exchanger between the arterial and venous bloods flowing in and out of the brain; 4) the high and constant arterial blood flow of the brain is sufficient to cool the brain under all conditions; and 5) the relatively low tympanic temperature (Tty) recorded in hyperthermic humans is not a sign of SBC, but rather is the sign of contamination of Tty by a low head skin temperature. These arguments are reviewed and rejected and results of several recent experiments are summarized. Finally, recent experimental articles that contradict the existence of human SBC or the validity of Tty are discussed and their conclusions refuted. This review points to overwhelming evidence in favor of human SBC.

The skin of the face is reputed not to vasoconstrict in response to cold stress because the face skin temperature remains steady during hypothermia. The purpose of the present work was to measure the vasomotor response of the human face to whole-body hypothermia, and to compare it with hyperthermia. Six male subjects were immersed in cold and in warm water to obtain the two conditions. Skin blood flow, evaporation, and skin temperature (Tsk) were recorded in three loci of the face, the forehead, the infra orbital area, and the cheek. Tympanic (Tty) and oesophageal (Toes) temperatures were also recorded during the different thermal states. Normothermic measurements served as control. Blood flow was recorded with a laser-Doppler flowmeter, evaporation measured with an evaporimeter. Face Tsk remained stable between normo-, hypo-, and hyperthermia. Facial blood flow, however, did not follow the same pattern. The facial blood flow remained at minimal vasoconstricted level when the subjects' condition was changed from normo- to hypothermia. When the condition changed from hypo- to hyperthermia a 3 to 9-fold increase in the blood flow was recorded. From these results it was concluded that a vasoconstriction seems to be the general vasomotor state in the face during normothermia.

The theory that stress (or emotional) rise in central temperature (Tc) in rats is a fever with an upward shift of the set-point temperature was tested with three experiments: 1) Measurement of tail skin temperature and Tc during the emotional Tc rise; 2) Investigation of the effect of ambient temperature on the emotional Tc rise; and 3) The assessment of emotional Tc rise during daytime and nighttime. Skin vasomotor responses helped the increase of Tc toward a higher level and contributed to the regulation of central temperature at this new higher level. The cold environment did not diminish the emotional rise of central temperature as it would be expected in the case of a hyperthermia. However, at night emotional fever reached a higher level than during the daytime, suggesting that prostaglandin rise in Tc is distinct from emotional or stress-induced hyperthermia. In conclusion, the experiments reported here confirm the hypothesis that the rise of Tc induced by handling or disturbance of the rats is regulated, and is due to a shift of the set-point as occurs in fever.

Gryllus bimaculatus were infected with an intracellular prokaryote, Rickettsiella grylli, then reared either at fixed temperatures or in a temperature gradient (22-36 degrees C) where they could select the temperature they preferred. Only 50% of the infected insects reared at 28 degrees C or less survived after 20 days, against 75% of those reared at 30 degrees C or more and 90% of those in the temperature gradient. Examination of smears of insect tissue showed that all (100%) of the infected insects reared between 23 and 29 degrees C had developed a strong rickettsial infection. Only 20% of the insects reared in a gradient of temperature showed signs of strong infection. Body temperature of crickets in the temperature gradient, recorded using thin thermocouples, was 33 degrees C in infected crickets and 26.6 degrees C in controls. It is concluded that thermoregulatory behavior was used by the insects to produce a fever when infected with Rickettsiella grylli. This protected them and increased survival capacity.

The direction of the blood flowing in the emissary veins (vena emissaria mastoidea and v. e. partietalis) was recorded in human subjects during moderate hyperthermia and hypothermia. During hyperthermia the blood flowed rapidly from skin to brain. During hypothermia either no flow could be detected or the blood flowed slowly from brain to skin. On two fresh cadavers the calvaria was removed with the scalp adhering. Gentle massaging of the scalp produced abundant drops of blood on the inner surface of the bone each time the scalp was massaged, thus showing that cutaneous blood can flow inward through the bone. These results support the hypothesis of selective brain cooling in hyperthermic humans by offering a possible mechanism.

1. Four subjects were immersed in a stirred water-bath maintained at either 30 or 40 degrees C. The left hand was placed out of the bath in a glove receiving water at a temperature selected by the subject as most pleasurable. Experiments were conducted during the euthermic state and during either spontaneous or induced fever.2. The results of control experiments confirm a previous observation using the same method, that preferred hand skin temperature was a linear function of internal temperature but also indicated an influence by mean skin temperature.3. The general pattern of response during fever was identical to that when fever was absent except that the regulated steady state internal temperature was higher and the slopes of preferred temperature plotted against internal temperature were steeper.4. The results seem to support the concept of a change in set point rather than that of a change in the gain of the thermoregulatory processes during fever.

The skin and colonic temperatures were recorded in frogs (Rana esculenta) which had selected a suitable microenvironment in a box filled with 2-3 cm water. The water temperatures ranged from 0 degrees C to + 40 degrees C. Such measurements were performed before and after intraperitoneal injections of killed pathogenic bacteria (M. xenopi and M. range), killed non-pathogenic bacteria (M. aquae II) and 0.9% sterile saline, intraperitoneal injections of blood plasma from frogs pre-injected with killed M. ranae, injections of PGE1 into the brain. The injections of pathogenic bacterial endotoxin caused, after latencies of 5-120 min, higher preferred water temperatures, which produced an average maximum colonic temperature increase of 6.5 degrees C +/- 1.0 degrees C (S.E.) (p less than 0.001). The non-pathogenic bacteria and sterile saline caused no temperature change. Monophasic hyperthermia of shorter latency was caused by injections of blood plasma from frog preinjected with M. ranae. Monophasic hyperthermia of the shortest latency was observed after diencephalic injections of PGE1. Based on their similarity we suggest that ectothermic and endothermic fever have a common phylogenetic origin.

1. Groups of aquatic snails (Limnaea auricularia) were placed in a temperature gradient and their thermopreferendum measured. 2. Injected with various amounts of killed Escherichia coli, bacterial endotoxin, human interleukin, and prostaglandin E1, E2 and F2 alpha, they did not develop a fever. 3. High doses of prostaglandins were toxic. 4. These results suggest that fever appeared in the course of evolution after the emergence of molluscs and before that of arthropods.