Hæmatoporphyrinuria and its relations to the source of urobilin / by David Fraser Harris.

  • Fraser-Harris, David Fraser, 1867-1937.
Date:
[1897]
Catalogue details

Licence: Public Domain Mark

Credit: Hæmatoporphyrinuria and its relations to the source of urobilin / by David Fraser Harris. Source: Wellcome Collection.

Provider: This material has been provided by The University of Glasgow Library. The original may be consulted at The University of Glasgow Library.

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    chief seat of the formation from haematin of the immediate ante- cedent of urobilin there can be no doubt, for (1) Increased destruction of red blood-discs in the liver, such as follows from injecting into the portal vein any substance which liberates Hb02, leads to an increase of urinary pigment. (2) In pernicious anaemia much iron is deposited in liver cells, and the urobilin is increased, indicating an exaggerated destruction of Hb02; in such urines the band at F can be seen (without con- centrating the urine), sometimes pathological urobilin, a more de- oxidised pigment, is formed due to the abnormally intense de- oxidative hepatic katabolism of Hb02. Since M'Munn made urobilin by oxidising acid-haematin by per-oxide of hydrogen, and then briefly de-oxidising with sodium- amalgam, he has suggested that «urobilin is formed by nascent oxygen in the tissues. As to the modus operandi of its formation there are, then, two theories : (1) The reduction theory; (2) The oxidation theory. Though most probably both reduction and oxidation occur in the formation of uroblin, neither is alone the method; and as it was unsatisfactory to attribute the reduction to intestinal nascent H, so it is unlikely that nascent oxygen in the tissues performs the oxidation. The living protoplasm of the tissues craves oxygen for itself, and fixes it interstitially If the Wis the great source of urobilin formation, it is, as we should expect, pre-eminently a region of de-oxidations. All other pigments are artificially produced by processes of more or less complete reduction, thus :— (1) Haematin acted on by nascent H = Haematoporphyrin. (2) Haematin (but not bilirubin) acted on by zinc + H2SO to full reduction, yields pathological urobilin, inter! mediate stages in this process giving « urobilinoidin (le Nobel), the chromogen of urohamatoporphyrin (3) Urobilin reduced yields pathological urobilin (para- urochrome). From these facts and other considerations we may follow M Munn in believing that the order of the pigments as to degree ol de-oxidation is as under: (1) Oxy-Haemoglobin. (2) Haemoglobin.