The pulse-rate, i.e. the rapidity of the heart's beats, is chiefly regulated by the inhibitory fibres of the vagus, although it is affected also by accelerating fibres. In the frog the latter, excepting those which pass to the motor ganglia of the heart from the endocardium, also run mainly in the vagus, which is really the vago-sympathetic (Gaskell). In the higher animals they run chiefly through sympathetic channels, though to a slight extent also in the vagus.

If we find that the administration of a drug quickens the pulse, we next try to discover the mode in which it has done so. A glance at the table (p. 293) will show that there are several ways in which acceleration may occur, though the most important is either paralysis of the vagus or, at least, cessation of its action. The usual stimulus to the vagus-roots in the medulla which calls the nerve into action is the pressure of blood within the medulla; when this is high the vagus-roots are stimulated, and the pulse becomes slow; when the pressure is low, the stimulus is removed, and the pulse again becomes quick. Alterations in the blood-pressure will therefore alter the pulse, and drugs which affect the arterioles may quicken or slow the pulse-rate without any marked action of their own on the heart or vagus. This has already been mentioned when speaking of nitrite of amyl, which, by lowering the blood-pressure, and thus lessening the normal stimulus to the vagus-roots, greatly quickens the heart in the dog (p. 288).

In order to ascertain whether irritation of the vagus has been caused reflexly or not, we may divide the nerves through which we may expect the reflex to have occurred, or we may abolish their action on the medulla to a great extent by the use of large doses of chloral.