THE CAPILLAKY CIRCULATION. 235 



the distended and altered walls of the capillaries, chiefly, at all events, at 

 the junctions of the epithelioid plates, into the lymph spaces beyond. This 

 is spoken of as the diapedesis of the red corpuscles. 



This latter " stagnation " stage of inflammation may be the prelude to 

 further mischief and indeed to the death of the inflamed tissue, but it, too, 

 like the earlier stages, may pass away. As it passes away the outlines of 

 the corpuscles become once more distinct, those on the venous side of the 

 block gradually drop away into the neighboring currents little by little 

 the whole obstruction is removed, and the current through the area is 

 re-established. 



The slowing and final arrest of the blood current described above is not 

 due to any lessening of the heart's beat ; the arterial pulsations, or at least 

 the arterial flow, may be seen to be continued in full force down to the 

 affected area, and there to cease very suddenly. It is not due to any con- 

 striction of the small arteries increasing the peripheral resistance, for these 

 continue dilated, sometimes exceedingly so. It must, therefore, be due to 

 some new and unusual resistance occurring in the area itself, and there can 

 be no doubt that this is to be found in an increased tendency of the 

 corpuscles, especially of the white corpuscles, to stick to the sides of the 

 vessels. The increase of adhesiveness is not caused by any change con- 

 fined to the corpuscles themselves; for if, after a temporary delay, one 

 set of corpuscles has managed to pass away from the affected area, the 

 next set of corpuscles brought to the area in the blood-stream is sub- 

 jected to the same delay and the same apparent fusion. The cause of 

 the increased adhesiveness must, therefore, lie in the walls of the blood- 

 vessels or in the tissue of which these form a part. That the increased 

 adhesion is due to the vascular walls and not primarily to the corpuscles 

 themselves is further shown by the fact that if in the frog, an artificial 

 blood of normal saline solution to which milk has been added be substituted 

 for normal blood, a stasis may by irritants be induced in which oil-globules 

 play the part of corpuscles, and by their aggregation. bring about an arrest 

 of the flow. 



We are driven to conclude that there exist in health certain relations 

 between the blood, on the one hand, and the walls of the vessel on the other, 

 by which the tendency of the corpuscles to adhere to the bloodvessels is kept 

 within certain limits; these relations consequently determine the normal 

 flow, with its axial stream and peripheral zone, and the normal amount of 

 peripheral resistance ; in inflammations these relations, in a manner we 

 cannot as yet fully explain, are disturbed so that the tendency of the 

 corpuscles to adhere to the sides of the vessel is largely and progressively 

 increased. Hence the tarrying of the corpuscles in spite of the widening 

 of their path, and finally their agglomeration and fusion in the distended 

 channels. 



We may add that the changes occurring in the vascular walls also at least 

 facilitate the migration of the corpuscles, and modify the passage from the 

 blood to the tissue of the fluid parts of the blood, the lymph of inflamed 

 areas being richer in proteids than normal lymph. 



We must not, however, pursue this subject of inflammation any further. 

 We have said enough to show that the peripheral resistance (and consequently 

 all that depends on that peripheral resistance) is not wholly determined by the 

 varying width of the minute passages, but is also dependent on the vital 

 condition of the tissue of which the walls of the passage form a part. When 

 the tissue is in health, a certain resistance is offered to the passage of blood 

 through the capillaries and other minute vessels, and the whole vascular 

 mechanism is adapted to overcome this resistance to such an extent that a 



