No abstract

Sensations evoked by thermal stimulation (temperature-related sensations) can be divided into two categories, "temperature sensation" and "thermal comfort." Although several studies have investigated regional differences in temperature sensation, less is known about the sensitivity differences in thermal comfort for the various body regions. In the present study, we examined regional differences in temperature-related sensations with special attention to thermal comfort. Healthy male subjects sitting in an environment of mild heat or cold were locally cooled or warmed with water-perfused stimulators. Areas stimulated were the face, chest, abdomen, and thigh. Temperature sensation and thermal comfort of the stimulated areas were reported by the subjects, as was whole body thermal comfort. During mild heat exposure, facial cooling was most comfortable and facial warming was most uncomfortable. On the other hand, during mild cold exposure, neither warming nor cooling of the face had a major effect. The chest and abdomen had characteristics opposite to those of the face. Local warming of the chest and abdomen did produce a strong comfort sensation during whole body cold exposure. The thermal comfort seen in this study suggests that if given the chance, humans would preferentially cool the head in the heat, and they would maintain the warmth of the trunk areas in the cold. The qualitative differences seen in thermal comfort for the various areas cannot be explained solely by the density or properties of the peripheral thermal receptors and thus must reflect processing mechanisms in the central nervous system.

We examined body core and skin temperatures and thermal comfort in young Japanese women suffering from unusual coldness (C, n = 6). They were selected by interview asking whether they often felt severe coldness even in an air-conditioned environment (20-26 degrees C) and compared with women not suffering from coldness (N, n = 6). Experiments were conducted twice for each subject: 120-min exposure at 23.5 degrees C or 29.5 degrees C after a 40-min baseline at 29.5 degrees C. Mean skin temperature decreased (P < 0.05) from 33.6 +/- 0.1 degrees C (mean +/- SE) to 31.1 +/- 0.1 degrees C and from 33.5 +/- 0.1 degrees C to 31.1 +/- 0.1 degrees C in C and N during the 23.5 degrees C exposure. Fingertip temperature in C decreased more than in N (P < 0.05; from 35.2 +/- 0.1 degrees C to 23.6 +/- 0.2 degrees C and from 35.5 +/- 0.1 degrees C to 25.6 +/- 0.6 degrees C). Those temperatures during the 29.5 degrees C exposure remained at the baseline levels. Rectal temperature during the 23.5 degrees C exposure was maintained at the baseline level in both groups (from 36.9 +/- 0.2 degrees C to 36.8 +/- 0.1 degrees C and 37.1 +/- 0.1 degrees C to 37.0 +/- 0.1 degrees C in C and N). The rating scores of cold discomfort for both the body and extremities were greater (P < 0.05) in C than in N. Thus the augmented thermal sensitivity of the body to cold and activated vasoconstriction of the extremities during cold exposure could be the mechanism for the severe coldness felt in C.

We investigated the thermoregulatory responses of sympathetic fibres supplying the tail in urethane‐anaesthetised rats. When skin and rectal temperatures were kept above 39 °C, tail sympathetic fibre activity was low or absent. When the trunk skin was cooled episodically by 2–7 °C by a water jacket, tail sympathetic activity increased in a graded fashion below a threshold skin temperature of 37.8 ± 0.6 °C, whether or not core (rectal) temperature changed. Repeated cooling episodes lowered body core temperature by 1.3–3.1 °C, and this independently activated tail sympathetic fibre activity, in a graded fashion, below a threshold rectal temperature of 38.4 ± 0.2 °C. Tail blood flow showed corresponding graded vasoconstrictor responses to skin and core cooling, albeit over a limited range. Tail sympathetic activity was more sensitive to core than to trunk skin cooling by a factor that varied widely (24‐fold) between animals. Combined skin and core cooling gave additive or facilitatory responses near threshold but occlusive interactions with stronger stimuli. Unilateral warming of the preoptic area reversibly inhibited tail sympathetic activity. This was true for activity generated by either skin or core cooling. Single tail sympathetic units behaved homogeneously. Their sensitivity to trunk skin cooling was 0.3 ± 0.08 spikes s−1°C−1 and to core cooling was 2.2 ± 0.5 spikes s−1°C−1. Their maximum sustained firing rate in the cold was 1.82 ± 0.35 spikes s−1.

No abstract

To investigate the characteristics of efferent projections from the preoptic area for the control of non‐shivering thermogenesis, we tested the effects of thermal or chemical stimulation, and transections of the preoptic area on the activity of interscapular brown adipose tissue in cold‐acclimated and non‐acclimated anaesthetized rats. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH) elicited non‐shivering thermogenesis in the brown adipose tissue (BAT); warming the preoptic area to 41.5 °C completely suppressed the thermogenic response. Injections of d,l‐homocysteic acid (DLH; 0.5 mm, 0.3 μl) into the preoptic area also significantly attenuated BAT thermogenesis, whereas injections of control vehicle had no effect. Transections of the whole hypothalamus in the coronal plane at the level of the paraventricular nucleus induced rapid and large rises in BAT and rectal temperatures. This response was not blocked by pretreatment with indomethacin. The high rectal and BAT temperatures were sustained more than 1 h, till the end of the experiment. Bilateral knife cuts that included the medial forebrain bundle but not the paraventricular nuclei elicited similar rises in BAT and rectal temperatures. Medial knife cuts had no effect. These results suggest that warm‐sensitive neurones in the preoptic area contribute a larger efferent signal for non‐shivering thermogenesis than do cold‐sensitive neurones, and that the preoptic area contributes a tonic inhibitory input to loci involved with non‐shivering thermogenesis. This efferent inhibitory signal passes via lateral, but not medial, hypothalamic pathways.

No abstract

To investigate the involvement of the medullary raphé in thermoregulatory vasomotor control, we chemically manipulated raphé neuronal activity while monitoring the tail vasomotor response to preoptic warming. For comparison, neuronal activity in the rostral ventrolateral medulla (RVLM) was manipulated in similar experiments. Injections of d,l‐homocysteic acid (DLH; 0.5 mm, 0.3 μl) into a restricted region of the ventral medullary raphé suppressed the tail vasodilatation normally elicited by warming the preoptic area to 42 °C. DLH injection into the RVLM also suppressed the vasodilatation elicited by preoptic warming. Injection of bicuculline (0.5 mm, 0.3 μl) into the same raphé region suppressed the vasodilatation elicited by preoptic warming. Bicuculline injection into the RVLM did not suppress tail vasodilatation. These results suggest that neurones in both the medullary raphé and the RVLM are vasoconstrictor to the tail, but only those in the raphé receive inhibitory input from the preoptic area. That input might be direct and/or indirect (e.g. via the periaqueductal grey matter).