CHAP, iv.] THE VASCULAR MECHANISM. 221 



together, so that their outlines are no longer distinguishable ; they 

 appear to have become fused into a homogeneous mass. Except in 

 cases where the stimulus produces permanent mischief, this peculiar 

 condition after a while subsides. The outlines of the corpuscles 

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

 gradually drop away into the neighbouring currents, little by little 

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

 re-established, and though the arteries and capillaries remain 

 dilated for some considerable time, they eventually return to their 

 normal calibre. 



The stasis, the arrest of the current here seen, 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 down to the affected 

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

 increase of peripheral resistance caused by constriction of the small 

 arteries, for these continue dilated rather than constricted. It must 

 therefore be due to some new and unusual resistance occurring in 

 the capillary area itself. The increase of resistance is not caused 

 by any change confined 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 is subjected to the 

 same delay and the same apparent fusion. The cause of the resist- 

 ance must therefore lie in the capillary walls, or in the tissue 

 of which they form a part. We are driven to conclude that the 

 walls of the capillaries (and of the other vessels) exert in health a 

 certain attraction on the corpuscles, maintain a certain adhesiveness 

 between them and themselves, thereby determining the normal flow, 

 with its axial stream and plasmatic layer, and offering a normal 

 resistance to the pressure of the arterial system; and that, in stasis, 

 for reasons which we cannot as yet explain, this attraction, this 

 adhesiveness is largely and progressively increased. Hence the 

 early disappearance of the distinction between the axial stream and 

 plasmatic layer, the tarrying of the corpuscles in spite of the widen- 

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

 even enormously distended channels. 



That the increased adhesion is due to the vascular walls and not 

 primarily to the corpuscles themselves is further shewn 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 through the capillaries. 



In true inflammation the course of events is different. The 

 vessels become dilated, but the loss of distinction between the axial 

 stream and the plasmatic layer does not occur. On the contrary 

 the plasmatic layer appears even more striking on account of the 

 large number of white corpuscles which gather in it and become 

 adherent to the inner surface of the walls of the veins and venous 



