THE PRODUCTION AND DISSIPATION OF HEAT 1107 



of the muscles and goose-flesh appearing at this time greatly aid in 

 sending the body-temperature upward. The height of the fever 

 having been attained, heat-dissipation more nearly balances heat- 

 production/ but is still inadequate to allow the abnormally large 

 amounts of heat to escape. During the last stages of fever, the pro- 

 duction of heat is diminished, while the dissipation of heat gradually 

 increases, owing to the reestablishment of a proper control over the 

 capillaries of the skin and the reappearance of the sweat. 



The underlying causes of fever having been established, the ques- 

 tion may now be asked how these changes are brought about. The 

 two most acceptable explanations are contained in the so-called neuro- 

 genic and toxogenic theories of fever. The former has been put forth 

 by Liebermeister^ and holds that the heat centers regulating the body- 

 temperature are raised to a higher pitch during fever, simulating our 

 means of adjusting the regulator of a thermostat in such a way that 

 the latter may yield a temperature of 40° C. instead of 35° C. In 

 accomplishing this end, the heat centers make use chiefly of the vaso- 

 motor and secretomotor mechanisms. In this restricted form this 

 theory seems to have little in its favor, but naturally, this statement 

 does not imply that the ordinary reflexes are excluded as adjunct 

 causative factors in the production of this form of hyperthermy. In 

 fact, the evidence is against such a view, because the brief febrile 

 reactions following the passage of biliary or renal calculi, catheriza- 

 tion, and various operative procedures, are undoubtedly produced by 

 a diminished loss of heat incited by the reflex constriction of the cuta- 

 neous blood-vessels. Hirsch, Miiller and Rolly^ have put forward the 

 view that fever results in consequence of a derangement of the meta- 

 bolic condition of the tissue cells by poisonous substances. This 

 explanation has much in its favor, and is well adapted to those febrile 

 reactions which follow upon the entrance of pathogenic bacteria into 

 the system. The implication is that the cells respond to these sub- 

 stances with an increased activity,^ thereby endeavoring to accomplish 

 some beneficial effect. Since the intake of food is much diminished 

 at this time, this metabolic augmentation is had mainly at the expense 

 of the organized constituents of the body. 



The preceding conclusion is upheld by the fact that fever greatly 

 affects the metabolism, but probably not so much its intensity as the 

 manner in which it involves the different foodstuffs. The deduction 

 that it is not merely a matter of intensity of oxidation, is upheld by the 

 fact that the amount of the oxidation products derived from febrile com- 

 bustions is very small, as well as by the fact that the respiratory quotient 

 remains practically unchanged.^ It appears, therefore, that these 



1 Krehl, Zeitschr. fiir allg. Physiol., i, 1902, 29. 

 8 Pathologie des Fiebers, 1875. 



3 Deutsch. Archiv fiir klin. Med., Ixxv, 1903, 265. 



4 Roily and Meltzer, ibid., xciv, 1908, 335. 



5 Senator and Richter, Zeitschr. fiir klin. Med., lix, 1904, 16. 



