288 EDEMA 



partial solution of the intracellular 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. 



Under pathological conditions increased permeability of the 

 capillary walls is probably one of the chief factors in the pro- 

 duction of certain forms of edema. We see evidence of it 

 particularly in inflammatory edema, with its proteid-rich ex- 

 udate. It cannot be doubted that in such conditions actual 

 physical alterations take place in the capillaries, when we see 

 that the slightly diffusible proteids 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 indistinguish- 

 able transition of such an inflammatory exudate into one con- 

 taining leucocytes and red corpuscles, which must pass through 

 openings of some kind in the vessels. Edema due to inflam- 

 mation and poisoning certainly depends to a large degree upon 

 alterations in the vessel- walls. The question remaining is, do 

 edemas that are not associated with distinct inflammatory or 

 toxic influences depend also upon the vascular permeability ? 

 does increased permeability ever lead to the formation of proteid- 

 poor transudates ? Cohnheim was inclined 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, leading to increased permeability ; or, whatimight amount 

 to the same thing, increased secretory activity of the endothe- 

 lium, as understood by Heidenhain, It is impossible at this 

 time to eliminate as non-existent this secretory-activity doctrine, 

 but, as we hope to show later, there exist other factors in all 

 these non-inflammatory edemas that are sufficient to account for 

 the edema without our having recourse to this hypothesis. For 

 the present, therefore, we may consider altered capillary perme- 

 ability as an essential factor in edemas characterized by 

 proteid-rich fluids (exudates), and state that the influence of 

 altered permeability in the production of proteid-poor fluids 

 (transudates) is not proved, and is perhaps not of impor- 

 tance. 



