The relations of cardiac hypertrophy to renal disease / by Robert Saundby.

  • Saundby, Robert, 1849-1918.
Date:
[1880]
Catalogue details

Licence: Public Domain Mark

Credit: The relations of cardiac hypertrophy to renal disease / by Robert Saundby. Source: Wellcome Collection.

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    elements, at least the enlargement was certainly not due to increase in the diameters of the tubules. The con¬ sequence of the imperfect compensation by hypertrophy of the other kidney caused in some cases death by acute or chronic uraemia, in others the animals continued to live, but were ill nourished until the deficit was covered by hypertrophy of the left ventricle. By careful estimations of the relative normal weights of the heart and kidneys, and comparison of these data with the weights of the altered organs, they were able to determine that the cardiac hypertrophy bore a definite proportion to the loss of renal substance, and therefore was truly compensatory for the renal defect. As a rule the heart was not dilated, in many the ventricle was in a state of spasmodic contraction, and they were unable to obtain any confirmation of Senator’s views already quoted relative to the pathogenesis of excentric and concentric hypertrophy. In those cases where cardiac dilatation oc¬ curred, the symptoms during life indicated a primarily defective or later destroyed compensation, the animals died with acute or chronic dropsy, and the weight proved imperfect compensation. In the case of a large black doe, which died with dropsy of all the serous cavities io days after the operation, the cardiac muscle was intensely granular, even after the addition of soda solution,. They regard this as evidence of the occasional occurrence of primary myocarditis. Much more frequently the myocar¬ ditis was secondary, but whichever it was it produced the appearance of “ excentric hypertrophy.” They were never able to obtain evidence of any increased blood pressure, but by careful measurements they determined a constant increase in the velocity of the circulation. Injections of urea also failed to produce a rise of blood pressuie, but stimulated the heart's action and quickened the blood stream.