Long before vaso-motor physiology had any place in science the pulse was known to afford valuable indications in disease. Either of the accessible arteries will answer instead of the radial; its convenience merely makes the wrist the common place of comparison. By careful examination of the pulse something may be learned of several of the factors concerned in its production. These factors are--1, the muscular force of the walls of the heart; 2, the state of the cardiac valves; 3, the muscularity of the arteries; 4, the elasticity of the arterial coats; 5, the state of the capillary circulation; 6, the qualities of the blood; 7, the condition of the nervous system as to excitability or apathy. A feeble heart must induce a feeble pulse. Moderate debility may be attended by slowness of the pulse, but usually a weak circulation is marked by frequent, small beats, like the vibrations of a short pendulum. A strong heart-beat (other things being equal) is relatively slow, with a proportionate pause after the second sound. {153} Valvular lesions produce various effects upon the pulse. Most notable are the irregularity connected often with mitral insufficiency and the jerking pulse (Corrigan) of aortic regurgitation. Believing, as the present writer does, in the existence of a true arterial systole following and supplementing the ventricular contraction,[38] it must be urged that a vigorous muscularity in the arteries promotes strength in the pulse--not by resistance, but by auxiliary propulsion of the blood. Another condition altogether is tonic, spasmodic contraction of the arteries. This is not often met with pure and simple, but a measure of it is seen in the corded or wiry pulse of acute enteritis or peritonitis. [Footnote 38: This view, although advocated by Sir Charles Bell, Legros and Onimus, Hermann of Zurich, and others, is opposed to the most prevailing vaso-motor physiology. Several complications and some contradictions in pathological discussion at the present time would be cleared up by the abandonment of the now commonly-held stopcock theory of arterial function, which has really nothing whatever to support it except the misinterpretation of some experiments upon arteries made many years since.] Deficient elasticity of the arteries is not easily separated in observation from muscular relaxation. When arteries undergo degeneration (atheromatous, fatty, or calcareous), their middle coat suffers the deterioration of both elastic and muscular tissues, these being substituted by materials either more or less yielding, and always less resilient, than the natural fabric of the vessels.