THE CAUSES OF EDEMA 343 



Just wliat chaii're.s are produced in tlie capillary walls that render 

 them more i)ermeal)le we do not know. Possibly in some instances it 

 is a partial solution of the intei-eellular cement substances, possibly 

 an enlargement of the stomata through loss of tonicity of the endo- 

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

 cells, or, as Heidenhain and Cohnheira thought, it may be a stinuila- 

 tion 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 colls, alter their structure and with that their permeabil- 

 ity. 



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 proteiijs escape 

 from the vessels in the same proportions as th&y exist in the plasma; 

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

 osmotic pressure, especially not Avhen Ave 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 permeability ever lead to 

 the formation of protein-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 w:as good evidence that the blood pressure alone could not 

 account foKthe edema, it was natural to Ascribe all these fornYs 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 

 by Heidenhain. It is impossible at this time to eliminate as yihn- , ; 

 existent this secretory-activity doctrine, but, as we hope to show later-, 

 there exist other factors in all these non-inflammatmy edtniQ^f^tlTat^"* 

 are sufficient to account for the edema without^ur ha^*ig r^jMirseto 

 this hypothesis. For the present, therefare. wt^-^jiay con>n#ler altered 

 capillary permeability as an essential factor in edema^^ characterized 

 by protein-rich fluids (exudates), and iglc'ffe^that'.tlie influence of al- 

 tered permeability in the producti^* of protein-poor fluids (trans- 

 udates) is not proved, and is perhaps not of importance, although 

 the evidence of recent studies on- experimental nephritis seems to 



