146 Disfurboiiccs of Circulation. 



ways some small anastomotic channels between adjacent terminal 

 arterial areas. Through such anastomoses, inappreciable under 

 normal conditions but distended by the collateral rise of blood 

 pressure when the embolism diverts the blood into the surround- 

 ing areas of distribution, the blood enters the infarct. The ques- 

 tion whether in any given case an embolism should cause an anaemic 

 or a hemorrhagic type of infarct is largely determined by the 

 texture of the tissue in which the lesion occurs, anaemic infarcts 

 being met in relatively firm tissues as in the kidneys, and haemor- 

 rhagic in looser structures as in the lungs. The explanation of 

 such distribution is not entirely clear but probably rests in the 

 facility afforded by the tissues at the border of the infarct for dis- 

 tension of the capillary anastomotic channels entering the infarcted 

 area. Naturally the looser the texture, the greater the ease of 

 such dilatation. It should however be realized that the collateral 

 congestion existing along the border of the infarct is productive of 

 swelling and of pressure upon the periphery of the infarct. 

 Granted a fairly firm structure, such pressure should compress the 

 very channels of ingress into the interior of the infarct which are 

 here supposed to give opportunity for the entrance of blood : and 

 in such instances the part occluded should remain anaemic. If. 

 however, the tissue be. loose in texture such compression cannot be 

 of sufficient importance to occasion the interference with these 

 anastomotic channels just suggested ; and here the blood may by 

 such paths enter the area from the zone of collateral hyperaemia 

 and give rise to the appearance of a haemorrhagic infarct. In- 

 farcts of the lung are usually haemorrhagic in type in conformity 

 with the natural looseness of this tissue ; but the writer recalls 

 a recent case of an anaemic infarct of a collapsed lung, bear- 

 ing out the above theory. There is no objection to the author's 

 views in so far as entrance of blood to the infarct through venous 

 anastomoses may constitute a part of the process ; but to the 

 writer's mind it is excessive to suppose that this factor with reflux 

 of blood into and through the venules and capillaries irom the 

 veins is the sole explanation of the phenomenon ; and in his opinion 

 both arterial and venous anastomoses may contribute, regulated 

 however by the factors of border swelling, texture of tissue and 

 pressure, to determine to what degree the entrance of blood may 

 be possible] . 



Microscopically a haemorrhagic infarct exhibits the capillaries of 

 the part turgid with blood and the lymph spaces and all the tissues 



