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We examined effects of the queen's presence on diurnal rhythms of temperature preference (TP) and locomotor activity (LA) in worker honeybees' groups. TP and LA of six queenless and six queenright (with the queen) groups of bees, consisting of 7-8 worker bees, were recorded in a thermal gradient system for four days, under light to darkness (LD) 12:12 photoperiod. The same experiments were conducted on five virgin queens (of the same age as those in the queenright groups), which were placed individually in the gradient chambers. The single virgin queens showed signs of distress and no rhythms of TP and LA. In contrast, there were diurnal rhythms of TP and LA in both group variants with daytime activity and nighttime rest. However, the queen's presence exerted a strong calming effect, reducing LA of bees both at day- and nighttime. The nighttime minimum LA of queenright groups was five times lower than that in queenless groups. Moreover, there was a reversal of the diurnal pattern of TP in queenright groups. The results are discussed in terms of the bee colony organization as a superorganism.

It is well known that decrease in body temperature provides protection to newborns subjected to anoxia/ischemia. We hypothesized that the normal body temperature of 33°C in neonatal rats (4°C below normal body temperature in adults) is in fact a preadaptation to protect CNS from anoxia and further reductions as well as elevations in temperature may be counterproductive. Our experiments aimed to examine the effect of changes in body temperature on oxidative stress development in newborn rats exposed to anoxia. Two-day-old Wistar rats were divided into 4 temperature groups: i. hypothermic at body temperature of 31°C, ii. maintaining physiological neonatal body temperature of 33°C, iii. forced to maintain hyperthermic temperature of 37°C, and i.v. forced to maintain hyperthermic temperature of 39°C. The temperature was controlled starting 15 minutes before and afterword during 10 minutes of anoxia as well as for 2 hours post-anoxia. Cerebral concentrations of lipid peroxidation products malondialdehyde (MDA) and conjugated dienes (CD) and the activities of antioxidant enzymes had been determined post mortem: immediately after anoxia was finished and 3, 7, and 14 days later. There were no post-anoxic changes in the concentration of MDA, CD and in antioxidant enzymes activity in newborn rats kept at their physiological body temperature of 33°C. In contrast, perinatal anoxia at body temperature elevated to 37°C or 39°C as well as under hypothermic conditions (31°C) intensified post-anoxic oxidative stress and depleted the antioxidant pool. Overall, these findings suggest that elevated body temperature (hyperthermia or fever), as well as exceeding cooling beyond the physiological level of body temperature of newborn rats, may extend perinatal anoxia-induced brain lesions. Our findings provide new insights into the role of body temperature in anoxic insult in vivo.

Terrestrial snails are often exposed to freezing. Therefore, we investigated seasonal shifts in hemolymph concentrations of cryoprotectants such as glycerol and glucose. We also investigated whether summer acclimation to cold and short-day photoperiod induced synthesis of cryoprotectants in Helix pomatia snails. Concentrations of the both cryoprotectants were elevated in winter and reduced in summer. These changes, however, were not correlated with shifts in liver glycogen content. Summer acclimation to cold (5 degrees C) and short-day photoperiod evoked a selective increase in glycerol concentration. In conclusion, glycerol may play a role in adaptation of the snails to winter cold and glucose is rather unlikely to provide the cryoprotection.

Various animals must cope with some specific extreme environmental conditions and, as a consequence, they developed extremely efficacious adaptive defence responses. The mechanisms of the specific defences are more clearly visible in some species than in humans. Therefore, animal models of the human defence mechanisms should be selected accordingly. The appropriate, well responding models may be regarded as "biological amplifiers". This review is focussed on examples of effective defence against: (i) parturitional asphyxia, which extends fertility of mammals; (ii) diving asphyxia, which extends access of food in aquatic birds and mammals; (iii) endotoxemia, which provides survival of the fittest in mammals showing top fertility; (iv) deep hypothermia, which enables hibernating mammals to arouse. Each of the defences needs close co-operation of the cardiovascular, respiratory and temperature regulatory systems. Underlined problems regarding a choice of appropriate experimental animal models should stimulate renaissance of comparative physiology.

Perinatal asphyxia in mammals leads to iron accumulation in the brain, which results in delayed neurobehavioural disturbances, including impaired learning and abnormal alertness over their entire life span. The aim of this investigation was to verify our hypothesis that newborn rats, showing reduced normal body temperature, are protected against neurotoxicity of the asphyxia up to senescence. Alertness was studied in adult and old male Wistar rats after exposure to critical neonatal anoxia: (i) at physiological neonatal body temperature of 33 degrees C, (ii) at body temperature elevated to 37 degrees C, or (iii) at body temperature elevated to 39 degrees C (the thermal conditions remained unchanged both during anoxia and for 2 h postanoxia). To elucidate the effect of iron-dependent postanoxic oxidative damage to the brain, half of the group (iii) was injected with deferoxamine, a chelator of iron. Postanoxic behavioural disturbances were recorded in open-field, elevated plus-maze, and sudden silence tests when the rats reached the age of 12 and 24 months. Open-field stress-induced motor activity was reduced in rats subjected to neonatal anoxia under hyperthermic conditions. In contrast, these rats were hyperactive in the plus-maze test. Both the plus-maze and sudden silence tests show reduced alertness of these rats to external stimuli signalling potential dangers. The behavioural disturbances were prevented by body temperature of 33 degrees C and by administration of deferoxamine.

Chronic experiments were conducted on five freely moving rabbits at ambient temperatures of 0-42 degrees Celsius. The influence of nasal mucosal thermal changes on the venous blood temperature inside the pterygoid plexus and on the temperatures at three intracerebral sites were investigated against the background of the carotid arterial blood temperature shifts. A correlation was found between: (i) the fluctuations in the nasal mucosal temperature reflecting its vasomotor responses, (ii) temperature shifts of the pterygoid plexus venous blood, and (iii) of the ventral brain. Mucosal vasodilatation caused parallel drops in both the plexal blood and brain temperatures. However, mucosal vasoconstriction was accompanied by increases in temperatures at those sites. Intracranial thermal shifts were independent of the arterial blood temperature changes. During motor activity in normothermia nasal mucosal vasoconstriction was present, and in that case brain temperatures exceeded arterial blood temperature. During rest, mucosal vasodilatation appeared and brain base cooled below the arterial blood temperature. During panting in dry heat, the brain base was cooler than the arterial blood by as much as 0.5 degree Celsius. The intensity of the selective brain cooling was directly proportional to deep body temperature. The blockade of the respiratory evaporation in heat elicited an increase of the plexal venous blood as well as brain temperatures above the arterial blood temperature. We conclude that the venous blood outflowing from the nasal mucosa exerts a cooling influence on the brain through the pterygoid plexus.

The hypothalamic-arterial blood temperature gradient (THpr-TAC difference) was studied on 10 freely moving rabbits at ambient temperatures between 0 and 42 degrees Celsius. In cold environment, below 10 degrees Celsius the THpt-TAC gradient varied considerably, but some distinct correlations were found between vasomotor responses of the nasal mucosa and fluctuations of brain temperature, as well as between vasomotor responses of the ear pinnas and changes of the arterial blood temperature. Vasodilatation of the nasal mucosa or the ear pinna caused respectively a drop in brain temperature or in arterial blood temperature. Opposite changes were induced by vasoconstriction in those areas. Variations in THpt-TAC gradient resulted from oppositely directed vasomotor responses in the nasal mucosa and in the ear pinnas. At high ambient temperatures above 35 degrees Celsius thermal panting was accompanied by selective brain cooling with respect to the arterial blood. Blocking the heat loss from the nasal mucosa caused an increase of the THpt-TAC difference, and under these conditions brain temperature was determined solely by arterial blood temperature. The assumed mechanism of the selective brain cooling in rabbits is the exchange of heat through the neurocranial bottom, between the ventral brain and the spacious splanchnocranial venous lakes supplied with blood from the nasal mucosa.