Key result
Smoking was associated with an attenuated increase in blood flux during thermal warming compared to non-smoking controls (P<0.005), indicating impaired microvascular function.
Why the study?
Does smoking history impair microvascular function and hyperaemic response to thermal warming compared to non-smokers?
Cross-Sectional (n=56)
Does smoking history impair microvascular function and hyperaemic response to thermal warming compared to non-smokers?
Smoking attenuates the sustained hyperaemic response to thermal warming, suggesting impaired microvascular function and reduced endothelial/smooth muscle cell activity that is evident even in younger smokers.
We have used laser Doppler fluximetry [LDF] and signal processing to investigate the effects of smoking on microvascular function. Skin bloodflux was measured using a pin-head probe [Moor Instruments, UK] mounted in a 1 cm heating block before and during mild thermal warming to 43 °C, in 8 heavy smokers [mean 50 y; 19 cigarettes/day, 30pack years], 20 light smokers [23 y; 11/day, 4 pack years] and their age, sex and BMI matched non-smoking controls. Basal LDF analysed in the time domain was similar in all 4 groups [10–15 AU]. The increase in blood flux during the initial 10 min heating was attenuated in both light and heavy smokers vs controls [P<0.005]. Total hyperaemic response [AUC to 10 min] was also significantly attenuated in the heavy smokers [4 ± 2 vs 6 ± 2 x10⁴ AU·sec] but not in the light smokers [8 ± 2 vs 10 ±4]. The LDF trace was analysed in the frequency domain using a fast Fourier transform and total spectral power together with the contribution of the frequency intervals between 0.01 and 2 Hz, calculated. Attenuation of the hyperaemic response in the heavy smokers was associated with a reduction in total spectral power of >40%, attributable to a reduction in spectral power around 0.01 Hz and 0.1 Hz [P<0.05]. These data suggest that the attenuation of the sustained hyperaemic response to thermal warming in long-term smokers is associated with a reduction in vasomotion and that this is in part the result of a reduced endothelial and smooth muscle cell activity. These changes are also evident in younger smokers with a shorter smoking history, suggesting that the vasodilatory response is impaired even at this early stage.
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Avery et al. (2006) conducted a cross-sectional in Microvascular dysfunction (n=56). Smoking vs. Non-smoking controls was evaluated on Increase in blood flux during the initial 10 min heating (p=<0.005). Smoking was associated with an attenuated increase in blood flux during thermal warming compared to non-smoking controls (P<0.005), indicating impaired microvascular function.
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