A STUDY I i\ M O U IJ 1 1) A N D X () 1! M A L 1' II V S I (> J. U V . Ifjo 



Time. Anr. Thess. Irritation. • UJiilAlilCS. 

 M. See. (Mill. metres.) 



4:20 -'9- 



4:25 30 



4:27 29 



6 30 



6:5 30 



6:15 30 Curruiit applied. Faradic current of the .«ame strcnztli as provinusly pmployod. 



6:20 34 Thv lower tracing of Fig. 6, Plate III. repiv.sei,ts tlie e.\i)eriinent, 



6:22 35 the second + belongs to it and mark.s the lieginninK of irritation. 



6:28 38 



6:32 40 A kink in tlie tube of artificial respiration apparatus monientarily 



6:34 43 interfered with the supply of air, causing partial asphy.via. 



6:39 38 



6:49 35 Current broken. 



"itS 33 Asjihyxia produced. 



7:10 42 



7:20 44 



7:22 44 Animal killed. 



In the first of tlie.se two experiments, the brain cortex having been destroyed 

 mechanically and the par vagnm cut, the arterial pressure rose, on galvanization 

 of the sciatic nerve, from 38 to 69 millimetres. After section of the splanchnics 

 the pressure rose from 17 to '29 millimetres on irritation of the sciatic, showing 

 that destruction of the cerebral cortex and of the splanclmics does not produce 

 complete vaso-motor palsy. Tlie comparative effects of irritation before and after 

 section of the splanchnics are well shown in Plate III., Figs. 1 and 2. The second 

 experiment was even more conclusive in its evidence. The stctidy arterial pressure, 

 after section of the splanchnics, was 31 to 33 millimetres. On galvanization of 

 the sciatic it rose in seven seconds to 35, and on production of asphyxia to 45. 

 The brain was then operated on, the Hitzig's cortex of both hemispheres being 

 removed, and on one side the ventricles being freely opened. The arterial pressure 

 at first fell to 29, but afterwards rose to 31. The scititic was irritated with a 

 Faradic citrrent of the same strength as before, and in seven seronds the pressure 

 rose to 35, and on asphyxia being induced increased still further to 45 (see Fig. 

 3, Plate III.). It is evident that in this case destruction of tiie cortex cerebri had 

 no effect upon the arterial pressure after the removal of the dominant influence of 

 the abdominal circulation, and it would seem as though vaso-motor influence must 

 be excluded from the explanation of the effects of wounds of this portion of the 

 cortex upon heat production. 



The opinion has already been expressed that the centre which directly controls 

 the production of animal heat is not in the cortex, consequently the fact that the 

 cortex has no vaso-motor action whilst it indicates the truth of the theory of a 

 direct nervous inhibition of heat production can hardly be considered to establish 

 it. Not knowing exactly in what region of the brain the sought-for calorific 

 centre, if it exists, is located, it is not possible to experiment directly upon the 

 effects of its destruction, but plainly the direct facts can be indirectly discovered 

 by studying the effect upon blood pressure of the galvanization of a sensitive nerve 

 after section of the medulla at its junction with the pons and of the splanchnics, 

 since such section removes the body from the influence of said calorific centre. 

 The following experiment is in such direction. 



