PATHOGENESIS OF EDEMA 343 



excessive escape of the blood fluids follows. Magnus also showed 

 that poisoning with arsenic, which injured the vessels, favored the 

 experimental production of edema by transfusion. Starling, as 

 noted before, observed that the permeability of the capillaries varies 

 normally in different organs and tissues, which dotorminos quantita- 

 tive and qualitative differences in the lymph normally flowing from 

 various vascular areas. Heidenhain's "lymphagogues of the first 

 class, " which are all poisonous substances, probably act by increasing 

 the permeability of the capillaries, and in this way they produce 

 local urticaria, which is often observed as a result of poisoning by these 

 same lymphagogues, e. g., shellfish and strawberry poisoning. Just 

 what changes are produced in the capillary walls that render them 

 more permeable we do not know. Possibly in some instances it is a 

 partial solution of the intercellular cement substances, possibly an 

 enlargement of the stomata through loss of tonicity of the endothelium 

 (Meltzer), sometimes it may be actual death of the endothelial cells, 

 or, as Heidenhain and Cohnheim thought, it may be a stimulation 

 of the endothelial cells to increased secretory activity. Fischer believes 

 that a change in the hydrophilic tendency of the colloids, induced 

 especially by acids formed in asphyxiated conditions of the cells, alter 

 their structure and with that their permeability. 



Under pathological conditions increased permeability of the capil- 

 lary walls is probably one of the chief factors in the production of 

 certain forms of edema. We see evidence of it particularly in inflam- 

 matory edema, with its protein-rich exudate. It cannot be doubted 

 that in such conditions actual physical alterations take place in the 

 capillaries, when we see that the slightly diffusible proteins escape 

 from the vessels in the same proportions as they exist in the plasma; 

 there can be here no question of heightened cell activity or increase in 

 osmotic pressure, especially not when we note the indistinguishable 

 transition of such an inflammatory exudate into one containing leu- 

 cocytes and red corpuscles, which must pass through openings of 

 some kind in the vessels. Edema due to inflammation and poisoning 

 certainly depends to a large degree upon alterations in the vessel- 

 walls. The question remaining is, do edemas that are not asso- 

 ciated with distinct inflammatory or toxic influences depend also upon 

 the vascular permeability? — does increased permeabiHty ever lead to 

 the formation of protein-poor transudates? Cohnheim was inchned 

 to attribute nearly all edema to this cause, for in passive congestion, 

 or nephritis, or any of the common causes of edema, it is easy to find 

 reason for the belief that poisons may be present in the blood; and 

 as there was good evidence that the blood pressure alone could not 

 account for the edema, it was natural to ascribe all these forms of 

 edema to the action of toxic substances upon the capillary walls, lead- 

 ing to increased permeability; or, what might amount to the same 

 thing, increased secretory activity of the endothelium, as understood 



