PATHOLOGICAL ANATOMY AX1) HISTOLOGY 205 



Sudan, Scarlet R. or Nile blue sulphate, or by examining sections by polar- 

 ized light for the determination of anisotropic lipoids. Such studies have 

 been carried out by Loescheke, Goldzieher, Thomas, Weltman, Elliott (g), 

 Kawamura and Landau (&). Others, notably Landau and McNee, have also 

 determined chemically not only the total lipoid but the amount of choles- 

 terol esters. From all these observations the general conclusion can be 

 drawn that in acute septic conditions and acute infections or acute intoxica- 

 tions, the lipoid disappears more or less rapidly; that in more chronic 

 infections it also disappears, but more slowly. In anemias and as a result 



Fig. 6. Section of suprarenal cortex showing granules. Case of pulmonary ab- 

 scess, abscess of liver, with general peritonitis. Stained with Mallory's phosphotungstic 

 hematoxylin. a. Intracellular granules with centers stained; b. Granule unstained. 

 Oil immersion photograph. 



of severe hemorrhage it also diminishes or disappears. On the other 

 hand, in all chronic circulatory conditions it is increased. This is 

 true not only for chronic renal conditions with hvpertrophied heart and 

 arteriosclerosis but also for cardiac conditions with decompensation. The 

 disappearance of the lipoid does not take place evenly throughout the 

 cortex. As the exhaustion advances one finds focal areas still loaded with 

 it whilst neighboring areas contain none. Finally only occasional cords 

 of the fasciculata contain lipoid and at last the whole cortex gives no 

 trace of lipoid material. We do not know really how these anisotropic 

 fats of the cortex pass from the cells to the circulation but before there is 

 complete exhaustion one sometimes sees in the neighborhood of the lipoid- 

 holding cells small groups of endothelial leucocytes which seem loaded with 

 fat, and this may be the method of transfer. Figs. 7 and 8 are low power 



