The causal role of tobacco in cardiovascular disease has been studied for years, and a number of investigations have been carried out to prove or disprove a relationship. It is now generally agreed that the large majority of normal persons respond to cigarette smoking with definite peripheral vasoconstriction, lasting from a few minutes to a half hour or even longer before the blood vessels gradually return to normal. In normal persons the usual vascular effects produced by the smoking of cigarettes include a rise in systolic and diastolic blood pressure, an increase in the pulse rate between 5 to 20 beats per minute, and simultaneous constriction of the peripheral blood vessels of the extremities, as measured by a decrease in cutaneous temperature. There is, however, considerable individual variation in physiological response to cigarette smoking.
Adequate evidence is available to demonstrate that the vascular effects are caused by nicotine. It has