Effect of smoking cessation on visually evoked cerebral blood flow response in healthy volunteers.

BACKGROUND/AIMS: In our previous study, impaired visually evoked flow velocity response was demonstrated in young chronic smokers. Our aim was to study whether impaired cerebrovascular reactivity is reversible 6-18 months after smoking cessation. METHODS: Flow velocity changes, evoked by visual stimulus, were recorded in the posterior cerebral arteries in 15 smokers, 15 former smokers and 15 nonsmokers. The stimulation protocol consisted of 10 cycles with a resting phase of 20 s (baseline) and a stimulating phase of 40 s for each cycle. Relative changes of flow velocity were expressed in relation to baseline. Breath holding index, visual evoked potential and intima-media thickness were also examined. RESULTS: Repeated measures ANOVA revealed marked difference in the flow velocity time courses between the 3 groups (p < 0.01). The flow response was significantly worse in former smokers than in nonsmokers (p < 0.002), however, no significant difference was found between former and current smokers (p = 0.0556). CONCLUSION: This is the first transcranial Doppler study demonstrating long-term impairment of visually evoked cerebrovascular response after smoking cessation. These findings indicate that the impairment of neurovascular coupling caused by smoking is due to structural changes of the vessels, rather than acute effect of smoking.

Acetazolamide-induced vasodilation does not inhibit the visually evoked flow response.

Different methods are used to assess the vasodilator ability of cerebral blood vessels; however, the exact mechanism of cerebral vasodilation, induced by different stimuli, is not entirely known. Our aim was to investigate whether the potent vasodilator agent, acetazolamide (AZ), inhibits the neurovascular coupling, which also requires vasodilation. Therefore, visually evoked flow parameters were examined by transcranial Doppler in ten healthy subjects before and after AZ administration. Pulsatility index and peak systolic flow velocity changes, evoked by visual stimulus, were recorded in the posterior cerebral arteries before and after intravenous administration of 15 mg/kg AZ. Repeated-measures ANOVA did not show significant group main effect between the visually evoked relative flow velocity time courses before and after AZ provocation (P=0.43). Visual stimulation induced significant increase of relative flow velocity and decrease of pulsatility index not only before but also at the maximal effect of AZ. These results suggest that maximal cerebral vasodilation cannot be determined by the clinically accepted dose of AZ (15 mg/kg) and prove that neurovascular coupling remains preserved despite AZ-induced vasodilation. Our observation indicates independent regulation of vasodilation during neurovascular coupling, allowing the adaptation of cerebral blood flow according to neuronal activity even if other processes require significant vasodilation.