Effect of cigarette smoking on basal and carbon dioxide stimulated cerebral blood flow in man.

Abstract

The effect of cigarette smoking on the basal cerebral blood flow (CBF) and on the cerebral hyperemia induced by CO2 breathing was investigated in healthy human volunteers. CBF was measured with the N2O-wash-in technique in the basal state and during inhalation of 5% CO2, before and after smoking of two commercial filter tipped cigarettes. In parallel the (arterial-jugular venous) difference in O2 content, arterial and jugular venous pCO2, pulmonary ventilation, heart rate and systemic blood pressure were followed. During smoking there was a 10-15 mmHg increase in systemic blood pressure and a parallel elevation of heart rate (+ 20 beats/min). Cerebral blood flow increased by about 25%, and cerebral vascular resistance fell about 15%. The cerebral metabolic rate of oxygen (CMRO2) was elevated by about 30% above control. Inhalation of 5% CO2 by itself markedly increased CBF and decreased cerebral vascular resistance, while leaving CMRO2 unaffected. Cigarette smoking did not significantly change either of these effects of CO2 breathing. From these data it is concluded that cigarette smoking elevates systemic blood pressure and decreases cerebral vascular resistance, and thereby augments basal CBF. This flow-promoting effect of smoking is probably due to an increased cerebral consumption of oxygen. Furthermore, the data demonstrate that smoking does not interfere with the cerebral vascular response to increased arterial pCO2.