388 Proceedings of Royal Society of Edinburgh. [sess. 
(3) Haematin. 
(4) Haematoporphyrin. 
Meio-de-oxyhaematoporphyrin. 
, Urohaematoporphyrin. 
Urobilinoidin. 
Urobilin. 
Urobilinogen. 
Para-urochrome (pathological urobilin). 
Para-urocbromogen. 
We have then to account for processes of decomposition, oxida- 
tion, and reduction in the transformation of blood-pigment to 
urinary-pigment. I believe it may be done thus : — 
Taking the liver in health, oxyhaemoglobin reduced is first de- 
composed to hsematin by separation of the proteid globin ; the 
haematin is, by separation of its iron, further decomposed into some 
antecedent of urobilin, perhaps its chromogen. 
This substance, secreted “ internally ” by the liver, passes on to 
the heart, and thence to the lungs, where it becomes oxidised to 
urobilin (hence the urobilin band in blood-serum*), and is then 
swept on into the arterial stream, to be (some of it) rapidly reduced 
at the moment of renal excretion ; hence we are prepared to find 
in urine some urobilin and some urobilinogen, which latter, as the 
urine stands, becomes oxidised to the pigment — a process hastened 
by the acid fermentation, or by the action of potassium perman- 
ganate, HC1 or HN0 3 on the urine. 
In pernicious anaemia the initial amount of this hepatic kata- 
bolism is increased, or is excessive in the degree of de-oxidation (as 
above indicated). On this view M‘Munn’s oxidation-stage by H 2 0 2 
has its analogy in the lungs, and his “brief reduction” by Ua-Hg 
in the kidneys. 
Bu-t there are probably other than hepatic sites of urobilin 
formation, and tissues other than the liver can to a certain extent 
transform haemoglobin. The blood of old clots (cerebral, aneu- 
rysmal, or of corpora lutea) often shows crystals of a proteid-free, 
iron-free pigment haematoidin (identical in analysis with bilirubin) ; 
blood effused into the peritoneum and other sites causes an increase 
* M‘Munn, Proc. pQy. Soc,, 1881, p. 231. 
