The effects of chronic cigarette smoking on cerebrovascular responsiveness to 5 per cent CO2 and 100 per cent O2 inhalation.

Abstract

Effects of chronic cigarette smoking on cerebrovascular responsiveness of volunteers at risk for stroke and not at risk for stroke were evaluated by serial measurements of cerebral blood flow using the 133Xe inhalation method. Resting gray matter blood flow values (Fg) measured while breathing room air were compared with Fg values measured during inhalation of either 5 per cent CO2 in air or 100 per cent O2. Changes in Fg values during inhalation of 5 per cent CO2 were used to estimate cerebral vasodilator capacitance, and those during inhalation of 100 per cent O2 were used to estimate cerebral vasoconstrictor capacitance. Results indicated that chronic cigarette smokers have both reduced vasodilator (P less than 0.01) and reduced vasoconstrictor (P less than 0.02) capacitance when compared with nonsmokers of the same ages regardless of whether or not other risk factors for stroke were present. Vasodilator capacitance to 5 per cent CO2 inhalation was reduced among smokers compared with nonsmokers of the same age by 48 per cent in non-risk subjects and 56 per cent in risk-factored subjects, while vasoconstrictor capacitance to 100 per cent O2 inhalation among smokers was decreased by 24 per cent in non-risk subjects and 34 per cent in risk-factored subjects. In risk-factored subjects, combined effects of smoking and other risks appeared to be additive.