Causes of the hypertrophy of the vascular system in granular degeneration of the kidney / by Robert Saundby.

  • Saundby Robert, 1849-1918.
Date:
1876
Catalogue details

Licence: Public Domain Mark

Credit: Causes of the hypertrophy of the vascular system in granular degeneration of the kidney / by Robert Saundby. Source: Wellcome Collection.

Provider: This material has been provided by the Royal College of Physicians of Edinburgh. The original may be consulted at the Royal College of Physicians of Edinburgh.

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    is not less, indeed it is more, frequent. ITypertropliy of the iirterioles is found in all cases where active liypeiccmia has long })crsisted, as in the brains of chronic maniacs, especially in that chronic parenchymatous intlammation of the brain occurring in general paralysis; in the neighbourhood of all chronic inflamma- tions, such as cir-rhosis of the liver, and, in all new formations of long standing, such as slowly-growing sarcomata. These appear- ances must be familiar to every microscopist, sfl I need not multi- ply instances. In all these the physical condition is the same—an increased local determination of blood stretching the vascular walls. We have therefore, as a constant antecedent, increased fulness of the vessels—a fulness, be it remembered, not quite unvarying in its amount, but somewhat intermittent, reaching its maximum as the column of blood receives the impulse from the contraction of the ventricle. But in granular kidney there is reason to believe that an increased fulness of the arteries is also a constant antecedent. Let us inquire whether this antecedent deserves to be considered an efficient cause of the general hypertrophy ; but before proceeding to do so, let me say a few words on the cause of this increased fulness. Local increased fulness may be caused in two ways: 1, by an in- creased quantity of blood going to the part; 2, by a diminution in the loss of plasma by exosmosis into the tissues of the part. The lirst condition is well recognised, and probably explains the local fulness in the cases instanced above; the second is not so generally recognised, but probably occurs and co-operates with the other in ■ the early stages of many hyperaeniim. But in general increased fulness of the vascular system, the fonner cannot obtain ; and the latter, diminished exosmosis, must be an important factor. In general fulness, moreover, another factor steps in, that is, increased endosmosis of fluid from the alimentary canal. The physical law regulating the passage of fluids of different densities separated by a membrane is, tliat a great deal of the less dense fluid will tend to pass into the space occupied by the more dense fluid, while a little of this latter will pass out into the less dense fluid. In the con- dition of tlie blood in granular kidney, have we not those physical conditions wliich, on tlie one hand, favour increased transudation of water from the alimentary canal, and, on the other, diminished exudation of plasma from the bloodvessels into the tissues V We know that in gout the blood contains large quantities of uric acid, find ])robably other ])roducts of tissue metamorphosis; in lithuria we may reasonably infer a similar condition; furthermore, people who suffer from lithuria are usually of sedentary habits, a large part of the protoplasm of their l)ody is in a comparatively quiescent state, not undergoing those active changes which call for constant su])])lies of nutrient plasma; furthermore, such a quiescent state ' I'lie dilution of the Idooil Ly endosmosis ^vi]l tend to readjust the cxosniosis IVoiii the vessels into the tissues ; indeed, ve may expect it to become greater tlian normal.