Formation of urobilin / by Vaughan Harley.

  • Vaughan Harley
Date:
1896
Catalogue details

Licence: Public Domain Mark

Credit: Formation of urobilin / by Vaughan Harley. Source: Wellcome Collection.

Provider: This material has been provided by King’s College London. The original may be consulted at King’s College London.

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    intestinal putrefaction. In consequence of the increased intestinal putrefaction which extended up the small intestine, urobilin was formed even in the small intestine, and so much so that nearly all the bile pigment was converted into urobilin before it left the intestines. The result obtained in this dog explains how in some human cases where there is increased intestinal putrefac- tion extending up the small intestine urobilin is formed high up in the small intestine instead of as, under normal cir- cumstances, commencing below the caecum. The increased urobilin in the urine would thus seem not only to be a pathological sign of increased bile in the intestinal tract, as pointed out by Muller, but also significant of increased putrefaction in the intestine. That intestinal bacteria are capable of converting bilirubin into urobilin has been long known, and is mentioned by Schmidt. In confirmation of the above results calomel gives us strong support. It is known that calomel, when given by the mouth, causes the fasces to contain large quantities of bile pigment, and it has generally been put down as signifi- cant of the increased flow of bile into the intestine and increased peristalsis along the intestinal tract. I have found in man that when small doses—| gr. or so— of calomel are given at frequent intervals, the stools by degrees assume a green colour and contain large quantities of bile pigment and only small quantities of urobilin, and in these cases the calomel causes no purging. As we know, calomel diminished the aromatic sulphates in the urine, and therefore diminished the intestinal putrefaction. The green stool of calomel is in all probability partly due to increased bile, but chiefly to the diminution of intestinal bacteria, the biliverdin in consequence not being converted into urobilin. Still further in support of the view that the increase of urobilin occurs in cases of increased intestinal putrefaction, I have found in one case since I obtained the above results, where there was a marked increase of aromatic sulphates there was also a great increase of urobilin. In fevers which are almost always accompanied by an increase of urobilin in the urine there is also an increase in the intestinal putrefaction; the same holds good for liver disease. In partial obstruction of the bile ducts the increased urobilin cannot be explained by increase of bile in the intestines, but seems to be the re'
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