iigo 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



The quantitative importance of endocrine modula- 

 tion of temperature regulation is more indisputable 

 when long-term conditions are considered. The 

 resting metabolic rate and the microscopic structure 

 of the thyroid gland vary with the time of the year in 

 animals (but not in man) ; cold induces increased 

 thyroid activity and this effect can be eliminated by 

 hypophysial stalk section (199), a phenomenon in- 

 dicating that it is elicited via hypothalamic structures 

 as in the above-mentioned acute experiments. Another 

 type of long-term adaptation of temperature regula- 

 tion is the change in furring which parallels climatic 

 changes in certain animals; this is also presumably 

 centrally controlled and hormonally elicited. The 

 process of hibernation represents the most extreme 

 type of such adaptation. 



An interesting example of changes in human tem- 

 perature regulation occurring simultaneously with 

 endocrine changes is the slight but relatively long- 

 standing rise in body temperature which appears in 

 women at the time of ovulation (19). 



A specific thermoregulatory hormone produced 

 in the thyroid gland and influencing tissue metabolism 

 with short-term effects has been proposed (14^, 143) 

 but its existence has not been confirmed (153, 201). 



Body Water Movements 



As shown by Barbour (11, 14), body water move- 

 ments occur during heat stress (hydremia with de- 

 creased diuresis) and cold stress (anhydremia with 

 increased diuresis) (i ). .An anhydremic reaction is also 

 seen in the beginning of fever and of muscular ex- 

 ercise when the body reacts as under cold stress until 

 the body temperature has ri.sen to a new balance 

 level. The anhydremia or at least decrease of plasma 

 volume in muscular exercise occurs rapidly, ap- 

 pearing within 5 mill, of moderate exercise (112). 

 In cold stress, water moves from the circulating 

 plasma to the extracellular or intracellular spaces, 

 particularly in the liver (12). 



The water-shifting response to cold stress is de- 

 pendent on the activity of the sympathetic ner\ous 

 system and disappears after cervical spinal transec- 

 tion (14) or after adrenalectomy (11). ^Vater shifting 

 can lie evoked by local thermal stimulation of the 

 base of the brain in the rabbit; it disappears in ani- 

 mals with chronic destruction of the anterior hypo- 

 thalamus (10, 11). The conclusion should be that the 

 water-shifting response is at least partly evoked by 

 the action of hypothalamic thermodetectors and is 

 coordinated by anterior hypothalamic structures. 



Simultaneous changes of water excretion point to 

 the participation of the supraopticohypophysial 

 system in this pattern of regulation. Local diathermic 

 warming of the detector region in the anterior hypo- 

 thalamus may produce an immediate reduction of 

 diuresis (183a), suggesting that this is a primary 

 thermoregulatory effector response and not secondary 

 to an increased \\ater loss. 



Ceie/jial and Spinal Pathways of Effector Systems 



Unilateral hypothalamic stimulation produces bi- 

 lateral responses from the thermoregulatory effector 

 systems. Hemitransection at the pontine level elimin- 

 ates contralateral sweating and diminishes ipsilateral 

 shivering and piloerection in the whole body of the 

 monkey (24). A similar effect is produced in the 

 lower extremities by hemitransection of the thoracic 

 spinal cord. The heat-loss effector systems project by 

 pathways which, according to studies involving 

 chronic lesions (25), can be anatomically separated 

 from the heat-production system (shivering) as high 

 as the mesencephalic le\'el (125), the former being 

 more medially situated than the latter. At the pontine 

 level heat-production mechanism paths are localized 

 within the cerebrospinal tract (127, 128) but, at the 

 lower cervical level of the spinal cord, these two tracts 

 are anatomically separated (48). 



TEMPER.'^TURE REGUL.ATION UNDER 

 .ABNORMAL CONDITIONS 



Effect of Anesthesia 



The effect of anesthesia (99, 162) is to suppress 

 temperature regulation, especially the cold response 

 mechanisms. Anesthesia therefore usually leads to a 

 slow fall of body temperature at effective surrounding 

 temperatures below 34° to 35 °C, the fall being pro- 

 portional to the depth of anesthesia and independent 

 of the nature of the anesthesia (fig. 21) (194}. Mag- 

 nesium ions have a similar effect (92). This rule has 

 exceptions: small doses (light anesthesia) of pento- 

 barbital inhibit the panting mechanism (140) and 

 lead to increased body temperature in the cat (60), 

 although not in the dog. On the other hand, the 

 hyperthermia in cats produced by hypothalamic 

 lesions is counteracted hv pentobarbital (168). After 

 the end of anesthesia, temperature regulation rapidly 

 improves but does not become normal until after 

 several hours (102). Ethyl carbamate (urethane) 



