A treatise on the principles and practice of medicine : designed for the use of practitioners and students of medicine / by Austin Flint.

  • Flint, Austin, 1812-1886.
Date:
1884
Catalogue details

Licence: Public Domain Mark

Credit: A treatise on the principles and practice of medicine : designed for the use of practitioners and students of medicine / by Austin Flint. Source: Wellcome Collection.

Provider: This material has been provided by the University of Massachusetts Medical School, Lamar Soutter Library, through the Medical Heritage Library. The original may be consulted at the Lamar Soutter Library at the University of Massachusetts Medical School.

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    urea, has not been establislicd. Voit found that symptoms resembling those ot uraemia are produced il the rapid elimination of urea fed to dogs be ))re- vented by withliolding water. The same etfects were observed after feeding in the same way some other substances, such as benzoate of soda. Voit there- fore does not attribute specific poisonous properties to urea, but thinks that ursemic symptoms appear when the accumulation in the blood of a variety of substances, including urea, uric acid, potash-salts, creatinin and extractive matters, becomes so great that the products of tissue-metamorphosis cannot Ite carried otF. These waste products collect, not only in the blood, but in tlie tissues, and here check that interchange between the tissue-elements and tlie nutritive fluids, which is essential to the proper performance of cell-function. The results hitherto obtained by experimentation with urea, cannot serve as a basis of support for the doctrine that urea is the sole poisonous agent in uraemia. The blood of ura^mic individuals has been analyzed with the view of deter- mining tiie injurious ingredients. The blood of animals, in which tlie kidneys have been extirpated or the ureters tied, has been found to contain urea in tenfold its normal amount, if the animals survive the operation two to tour days. These experiments show that urea is not formed exclusively in the kidneys, but tliat it is produced elsewhere and conveyed to these organs by the blood. Normal blood contains 0.01 to 0.08 per cent, of urea. The quantity of urea has been found much increased in the blood of urjemic patients. Bartels mentions a case in which 0.8 per cent, of urea was found. Hoppe-Seyler found 0.127 per cent. Tliese amounts are larger than has usually been found in urtemia' But other excrementitious substances as well as urea are present in excess. A notable increase of extractive matters (0.8G per cent., Hoppe-Seyler) has beep found, the importance of which is not to be underestimated because they have hitherto defied chemical analysis. There is one factor which disturbs the cer- tainty with which urea accumulates in the blood when the function of the kidneys is suspended, namely, the vicarious elimination of urea by other organs. Urea may be excreted vicariously by the stomach, intestine, and skin. It has also been found in larger percentage in dropsical effusions than in the blood. In the stomach and intestine urea is readily converted into carbonate of am- monia. Urea has repeatedly been observed in uraemia as a crystalline deposit u})on the skin. The bile has been found to contain an abnormal amount of urea. While urea has been found in excess in ursemic blood, there have been also cases of urgemia in which the amount of urea in the blood has been slightly, if at all, increased. In one case, Jacobsen' found the quantity of urea too small to admit of quantitative estimation. On the other hand, a large quantity of urea has been Ibund in the blood without the coincidence of ursemic symptoms. Unless in these analyses there has been some error, it seems quite certain that there are cases of urjemia in which the symptoms are not due to the retention of urea in the blood. A theory of uraemia elaborated by Frerichs with great skill, which obtained at one time considerable credence, is now generally discredited, at least, as regiirds its applicability to most cases This theory is, that uraemic symptoms are due to the presence, in the blood, of carbonate of ammonia pr-^duced by decomposition from the urea. There is no evidence for Frerich^'s assumption that urea is decomposed into carbonate of ammonia in the Mood. This de- composition, however, takes place in the stomach and intestine, carbonate of ammonia having been recognized often in the vomit of uremic patients. ' Ziemssen's Cyclopaedia of the Practice of Medicine, English translation, vol. xv. p. 130.