CENTRAL NERVOUS REGULATION OF BODY TEMPERATURE 



I181 



gators (74, 75, 133), such is not the case. Species 

 differences may exist, as chronic spinal dogs appar- 

 ently do not show active temperature regulation (45, 

 cf. 193, however). If satisfactory histological control 

 of the completeness of transection is made, a positive 

 result of such experiments should weigh more than a 

 negative result, as coinplications such as infection or 

 bleeding locally around the transection, and perhaps 

 undernourishment, imbalance of water and elec- 

 trolytes, etc., may occur which can result either in a 

 larger destruction than attempted or diminish the 

 responsiveness of the thermoregulatorv effector sys- 

 tems. The conclusion therefore should be that chronic 

 spinal animals may regain some power of active tem- 

 perature regulation, although ineffective in com- 

 parison to that of intact animals. 



Chronic high mesencephalic transections have 

 also been reported to leave traces of functioning 

 temperature regulation (concerned with heat-loss 

 mechanisms) intact, suggesting that structures caudal 

 to the hypothalamus may have an integrative thermo- 

 regulatory function. A possible explanation for the 

 discrepancy between the results of chronic hypotha- 

 lamic lesions and chronic mesencephalic transection 

 may be that in the former experiment cortical in- 

 fluences remain which are excluded in the latter. In 

 evaluating these positive results of chronic tran- 

 section experiments, their implication for normal 

 temperature regulation should be judged cautiously. 

 Even if central temperature regulation can be exerted 

 to a measurable degree by spinal structures when they 

 are freed from cerebral influence, their quantitative 

 role in the intact animal remains unknoAvn. 



THERMOREGUL.\TORV EFFECTOR SYSTEMS 



Respiration 



The respiratory system has pulmonary gas ex- 

 change for its main function, and both respiratory 

 rate and depth are therefore mainly regulated to 

 adapt alveolar ventilation to the metabolic needs of 

 the body. In addition, dead space ventilation serves 

 as an important thermoregulatory mechanism in most 

 animals, heat load producing rapid shallow breathing, 

 culminating in panting. These two mechanisms may 

 conflict in the intact animal. A typical example is 

 the increase in alveolar ventilation which occurs in 

 anoxia and which decreases the ability of the bodv to 

 preserve heat under cold stress (72, 76, 132). Another 

 example is emotional or sexual activation which is 



accompanied by prominent respiratory reactions 

 which can be seen in an exaggerated fashion in the 

 chronic decorticate animal (17, 18). In man, tiie 

 responses to overheating may induce true hyperpnea 

 with increased alveolar ventilation and eventually 

 hypocapnia and alkalosis (19). 



•Signals both from surface thermoreceptors and 

 from central thermodetectors contribute to evocation 

 of thermal panting; the cjuantitative importance of 

 tiiese two factors (32, 135) is difficult to judge and 

 probably varies considerably between species. In 

 some species, notably the dog, panting may start 

 when the animal expects to start muscular exercise, 

 when it is exposed to sunshine before body tempera- 

 ture rises (93) or when it is emotionally excited. 

 Panting can also be evoked as an experimentally 

 conditioned reflex (93). It may be concluded there- 

 fore that cortical mechanisms in some animals may 

 incite panting. This is reasonable although it is 

 difficult to elicit panting by electrical stimulation of 

 the cortex. On the other hand, periods of panting un- 

 related to heat stress may occur in the decorticate 

 animal which suggests that the cortex normally also 

 exerts a modifying or suppressing influence. Decorti- 

 cate panting may be dependent on structures in the 

 dorsocaudal diencephalon (134) [although the evi- 

 dence is controversial (53)] and may remain after 

 ablation of the larger part of the hypothalamus (fig. 

 10). 



Hypothalamic warming (fig. 2) and electrical 

 stimulation (fig. 11) can produce panting. In the 

 anesthetized animal it appears more easily when the 

 respiratory resistance is low, as when the trachea is 

 cannulated or when the mouth is kept open. It ap- 

 pears at a higher hypothalamic temperature than 

 does cutaneous vasodilatation (fig. 12). After high 

 mesencephalic transection, panting can only 

 exceptionally be evoked (123, 154). Chronic hypo- 

 thalamic lesions also extinguish the panting mecha- 

 nism (fig. 13), even if the cortex is intact. The con- 

 clusion is that hypothalamic structures are the most 

 important for the coordinated panting mechanism 

 but that other structures (cortical, dorsal dien- 

 cephalic) may also play a part by conditioning either 

 the hypothalamic or the bulbar-medullary respiratory 

 relays. In chronic spinal animals, panting occurs at a 

 higher body temperature than in intact animals (35), 

 illustrating the influence of the surface thermore- 

 ceptors which were deafferented by the transection. 



Bulbar respiratory mechanisms are influenced by 

 changes of body temperature, as is evident in animals 

 with chronic mesencephalic transections (33), even 



