CENTRAL NERVOUS REGULATION OF BOD"*' TEMPERATURE 



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FIG. 19. Effect of hypothalamic warming (as in fig. 17) on 

 cortical electrical activity from the left temporal area. Rabbit is 

 under urethanc anesthesia. Temperature of the hypothalamic 

 heating electrode {H.T.), ear-skin temperature (E.T.) and 

 respiratory rate are shown. Intense warming produces desyn 

 chronized cortical activity and 'emotional' polypnea, but no 

 cutaneous vasodilatation. [From von Euler & Soderberg (208).] 



perature. This might, e.g., explain why hyperphagia 

 and a steady liyperthermia may appear together 

 after hypothalamic lesions (145). 



From a conceptual point of \iew this suggestion is 

 a definite advance. The central nervous thermo- 

 regulatory mechanism has sometimes been coinpared 

 to a thermostat; in fever and during hard muscular 

 work (152) when thermoregulatory balance is 

 achieved (20) at a higher le\el of body temperature 

 than is normally the case at rest, the 'thermostat' 

 is said to be 'reset.' A given intensity of muscular 

 work leads in man to an ultimate new level of body 

 temperature (152) which is relatively independent of 

 the surrounding conditions for heat loss, an observa- 

 tion demonstrating that the body regulates by ad- 

 justing its heat-loss mechanisms at the new level. If 

 under such conditions the activities of the different 

 thermoregulatory effector systems can be stated 

 quantitatively and the central reference mechanism, 

 the brain-stem activating system, responsible for the 

 new thermoregulatory balance can be defined, the 

 terms 'thermostat' and 'resetting' would certainly 

 have an explicit meaning. 



Humoral Effector Systems 



When a skin area is cooled, a refle.xly induced 

 activation of the adrenal meduUae occurs with aug- 

 mented secretion of sympathetic catechol amines 

 (61). Intravenously administered epinephrine has a 

 significant calorigenic (glycolytic) effect and has 

 therefore been suggested to play a role in temperature 

 regulation, but opinions differ as to its quantitative 

 importance (138). Epinephrine and norepinephrine 



also constrict skin arterioles which would be an addi- 

 tional thermoregulatory effect, but the adrenal hu- 

 moral control of peripheral vessels is quantitatively 

 unimportant in comparison with their nervous vaso- 

 constrictor control (42, 67). The adrenal medullae 

 are under hypolhalainic control but the possible 

 coordination between adrenomedullary activity and 

 the thermoregulatory effector systems is not well 

 known (46). 



Extirpation of the thyroid gland (119, 159), the 

 adrenal glands or the hypophysis (31, 179) influences 

 temperature regulation, reducing resistance to body 

 cooling and the intensity of the fever response to 

 pyrogens (77). This fact is not in itself sufficient proof 

 that these endocrine glands take part in short-term 

 temperature regulation in the intact animal. The 

 extirpation effects might be attributed to a slowly 

 changed reactivity of thermoregulatory effector 

 organs, such as the blood vessels, to their normal mode 

 of control. Direct evidence in acute experiments, 

 however, demonstrates that exposure to cold within a 

 few hours evokes an increase of thyroxin secretion from 

 the thyroid gland of rabbits (37). After a further 

 latency the metabolic rate of the body responds by an 

 increase. This thyroid-activating effect of acute cold 

 exposure is mediated via the hypothalamohypophysial 

 connection (205). Local heating of the anterior hypo- 

 thalamus has been reported to decrease the blood 

 flow through the thyroid gland (183). 



A relatively imtnediate effect on temperature reg- 

 ulation seems to be exerted by the adrenocorti- 

 cotrophic hormone (ACTH) which induces hypo- 

 thermia in the normal rabbit (fig. 20) and counteracts 

 pyrogen fever (58). 



HOURS 



FIG. 20. Average change of body temperature in two rabbits 

 after intravenous injection of posterior pituitary extract (o. i 

 units per kg) or adrenocorticotropic hormone (ACTH) (i unit 

 per kg). [From Douglas & Paton (58).] 



