354 Dr. A. du Pre Denning and Mr. J. H. Watson. [May 7, 



gradually encroached upon. We know that the rate of flow in capillaries is 

 much slower than in the arteries and veins., tor it is here that the greatest 

 resistance is met with, and consequently most of the driving pressure is 

 spent ; if, therefore, the arteries leading to the capillary area are contracted 

 in the slightest degree the sum total of the increased resistance in such an 

 extensive change as occurs in Bright's disease must make a very marked 

 difference in the work necessary to bring about a minimum circulation 

 through the capillaries, that is to cause a blood velocity of the order of 

 - 5 mm. per second. We have already seen that the frictional resistance 

 produced by alteration in the smaller capillary bores increases very rapidly 

 with diminution in size, more especially with the finer periphery vessels. In 

 order, therefore, that the mechanism be fully compensated for the narrowing 

 of the smaller channels, there must be either: (1) an increase in the driving 

 force, that is, a more powerful heart beat, or (2) a diminution in the viscosity 

 of the blood itself. As is well known, the compensation in Bright's disease 

 is usually brought about by an hypertrophy of the heart itself ; and apart 

 from any changes which may occur in the constitution of the blood (which 

 indeed often shows an increased viscosity) we consider that the enormous 

 increase in peripheral resistance occasioned by the general con- 

 traction of the smaller vessels affords an ample explanation of the vexed 

 cpiestion of the cause of cardiac hypertrophy which is so truly necessary to 

 bring about an adequate circulation. Furthermore, we do not see any reason 

 to reinstate Bright's theory that there is some unknown substance circulating 

 in the blood which acts directly on the heart muscle, as Hirsch and Beck have 

 recently attempted. 



Effect of Changes in the Composition of the Blood. — With regard to the 

 changes in the composition and constitution of the blood, which will give 

 rise to variations in the viscosity and, as a consequence, affect the circulatory 

 mechanism, one can only remark here upon their infinite variety. Taking 

 the plasma alone there may be (1) an increase or diminution in its volume ; 



(2) proteid strength may be altered ; (3) salts may be deficient or in excess ; 

 (•1) metabolic products, e.g., alloxuric bases and other nitrogenous derivatives 

 abnormally abundant ; (5) excessive saturation with gas, for instance CO2 ; 

 (6) presence of ferments, organised and unorganised. All these in themselves 

 are capable of altering the viscosity values. 



Or again, if we consider the corpuscles, viscosity changes can be produced 

 by (1) variations in number of reds; (2) variations in number of whites; 



(3) variations in size. 



We may here make mention of the following interesting experiments of 

 Ferrai on the viscosity of the blood in partly asphyxiated animals. In his 



