LYMPH FORMATION AND CIRCULATION 121 



to the amount of salt in the diet. A very considerable retention of 

 water usually occurs before there is any evidence of edema; indeed, as 

 a result of giving salt, the body weight may increase from five to seven 

 kilograms (10 to 15 pounds) within a day or two without the appear- 

 ance of puffiness. 



The cause of the edema during salt retention is no doubt closely re- 

 lated to the action of lymphagogues. In a normal person excessive in- 

 gestion of salt is immediately followed by excretion of the excess through 

 the kidney. Where the kidneys are diseased, this excess of salt is re- 

 tained in the blood, raising its osmotic pressure and attracting water 

 from the tissue fluids. This leads to excessive thirst, the imbibed water 

 being used to replace that lost from the tissues. But all the crystalline 

 lymphagogues do not, when present in excess in the blood of nephritic 

 patients, necessarily cause edema; urea, for example, may accumulate 

 considerably without any such effect. The different action is usually 

 attributed to inequality in the diffusibility of the two crystalloids through 

 animal membranes, sodium chloride diffusing much less readily than 

 urea. 



It is most important to note that the fluid in edema is loose in the 

 tissues and can be drained away by the insertion of tubes. There is 

 absolutely no evidence in support of the claim of Martin Fischer that 

 edema is due to imbibition of water by the colloids of the tissues. This 

 question has been fully discussed elsewhere (page 62). 



BLOOD AND LYMPH REFERENCES 



(Monographs) 



iHowell, W. H.: The Harvey Lectures, J. B. Lippincott Co., xii, 271'. 



^Starting, E. H.: Human Physiology, Lea & Febiger, 1915. 



sRowe, A. H.: Arch. Int. Med., 1917, xix, 354, 



^Williamson, C. S.: Arch. Int. Med., 1916, xviii, 505. 



sTower and Herm: Proc. Soc. Biol. and Med., 1916, xviii, 505. 



eRous and Robertson: Jour. Exp. Med., 1916, xxiii, 219, 239, 549 



TButler, G. G.: Quart. Jour. Med., 1912, vi, 145. 



SHowell, W. H.: cf. Harvey Lecture; also Am. Jour. Physiol., 1913, xxxii, 264. 



^Drinker, C. K., and K. E.: Am. Jour. Physiol., 1916, xli, 5. 

 loDenny and Minot: Arch. Int. Med., 1916, xvii, 101; Ain. Jour. Physiol., 1915, 



xxxviii, 233. 



"Addis, T.: Quart. Jour. Med., 1910, iv, 14. 



"Cannon and Mendenhall: Am. Jour. Physiol., 1914, xxxiv, 225. 

 isHowell, W. H.: Arch, Int. Med., 1914, xiii, 80. 

 "Brodie, T. G.: Jour. Physiol., 1897, xxi, 403. 



isWhipple, G. H.: Arch. int. Med, 1912, ix, 365; Jour. Exp. Med.. 1911, xiii, 136. 

 leWhipple, G. H.: Arch. Int. Med., 1913, xii, 637. 

 "Duke, W. W.: Arch. Int. Med., 1912, ix, 258. 



