118 THE ADRENALS AND THE RESPIRATORY BLOOD-CHANGES. 



Miiller, can do but one thing: i.e., block the normal functional 

 cycle. Urobilin will of necessity disappear from the faces and 

 from the urine, since the functions of the organism will con- 

 tinue; and, retransformed into bilirubin, the pigment, in its 

 turn, must accumulate in the organism behind the obstruction. 

 It is for this reason, therefore, that "the tissues remain loaded 

 with bilirubin." The close relation between haematoporphyrin 

 and bilirubin further affirms itself when we compare their 

 formulae : 



C 32 H 32 N 4 5 C 32 H 36 N 4 6 



Haematoporphyrin. Bilirubin. 



When we consider that the latter differs only from the former 

 by a surplus of oxygen and hydrogen (C 32 H 32 N 4 5 -f 2H 2 

 = C 32 H 36 N 4 6 ), we are reminded of the avidity of the tissues 

 for oxygen, referred to when the blood-changes leading to 

 haematoporphyrinuria were analyzed. We then noted that the 

 tissues, in the absence of oxygen, took the place of the labora- 

 tory acid which removed oxygen from haemoglobin, leaving a 

 chromogen which slowly lost its iron, and which, minus its 

 iron, became iron-free haematin, or haematoporphyrin. But we 

 must remember, in this connection, that the reaction given as 

 illustration refers to a laboratory operation and to sulphuric 

 acid or an equally powerful reagent, and that in the tissues 

 the avidity for oxygen continues when blood-disintegration has 

 reduced respiratory oxidation to a minimum just compatible with 

 the continuation of life, and they continue, nevertheless, their 

 deoxidizing effect, more and more depleting the blood of its 0. 

 In the majority of diseases attended with blood-disintegration 

 we do not meet with hcematoporphyrinuria, therefore, but with 

 urobilin in the urine and stercobilin in the faces, both being 

 formed when the first named or its isomer, bilirubin, are ex- 

 posed to putrefactive processes, etc.; so that we do witness 

 haematoporphyrinuria, though slightly modified, with great 

 frequency. The suprarenal insufficiency involved also reduces 

 the normal formation of oxyhaemoglobin, but to a less marked 

 degree, probably because the disease is not complicated with 

 adrenals previously weakened by advanced disease, and the 

 avidity of the tissues is correspondingly less. Instead, there- 



