 
        Excerpt from The Monthly Abstract of Medical Science, Vol. 6: January, 1879
The significance of the first point investigated - the effect of the valvular lesion upon the blood-pressure - is very important. The same forward movement of the blood will require an increased exertion of the muscular tissue of the heart, if a resistance is interposed, as in stenosis, or an increased mass of blood has to be moved, as in regurgitation through the aortic orifice. If this increased power is brought into Operation gradually, in consequence of an increase in the muscular tissue - hypertrophy, etc. - the. Damage to the valve will be followed immediately by a greater or slighter fall in the arterial pressure. The answer which experi ment gives to the question is that there is no such fall. Before and after the operation the blood-pressure is precisely the same. Moreover, immediately after great valvular damage, the blood-pressure may be a little higher than before the operation, probably in consequence of the mechanical irritation of the muscular tissue of the heart-muscle, or of a reflex stimulation through the vase-motor nerves. When this immediate disturbing effect has passed away the pressure is found to be just the same. The permanent over-action of the heart necessary to maintain the blood-pressure leads to its hyperaophy. The reserve of force which the heart pomesses enables it to maintain its due action from the first. This effect is the same whether the valvular change is one by which obstruction or incompe tence is produced. It is evident, therefore, that the latent reserve of cardiac force is a very large one, and the reserve is manifestly of paramount importance for the maintenance of the circulation. Several of rosenbach's experiments show that this reserve maintains the pressure, even in the face of grave valvular damage, for many weeks - until, indeed, hypertrophy is developed. The details of the experiments prove that in all cases the first structural change was dilata tion, and that the hypertrophy was secondary in time to the dilatation, but never suficient to effect a perfect structural compensation, although dynamically the compensation was complete. Another point of interest is that there was very constantly developed an aneurismal dilatation of the apex of the heart, and also a fibrous degeneration of the mitral papillary muscle.
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