In most infectious disease there is a progressive fall in blood-pressure during the course of the infection. This fall has been attributed to a weakness or insufficiency of the circulatory apparatus. In 1899 Romberg, Pässler, Bruhns and Müller1 investigated the cause of this presumed weakness by means of animal experiments. They reached the conclusion that the myocardium was not at fault but that the toxin of the infection caused a grave injury to the vasomotor center in the medulla, and that the low pressure was due entirely to an abeyance of the function of this center. Since that time it has been generally held by clinicians that the height of the blood-pressure in the infectious diseases was a measure of the tone of the vasomotor center, that low readings were evidence of the failure of the center and were an absolute indication for therapeutic procedures which stimulated the center.