TY - JOUR
T1 - Cigarette smoking is associated with an acute impairment of microvascular function in humans
AU - Ijzerman, Richard G.
AU - Serne, Erik H.
AU - Van Weissenbruch, Mirjam H.
AU - De Jongh, Renate T.
AU - Stehouwer, Coen D.A.
PY - 2003/3/1
Y1 - 2003/3/1
N2 - An effect on microvascular function has been proposed as a possible mechanism explaining the association of acute smoking with increased blood pressure and decreased insulin sensitivity. However, the effects of smoking on microvascular function have not been studied. We have investigated the acute effects of smoking on microvascular function in 12 healthy smokers. Before and after smoking a cigarette, we measured heart rate, blood pressure and capillary recruitment during peak reactive hyperaemia. We also measured endothelium-dependent and endothelium-independent vasodilatation of the skin microcirculation with iontophoresis of acetylcholine and sodium nitroprusside respectively combined with laser Doppler fluxmetry. To exclude non-specific changes, a control study with sham smoking was performed. The smoking and sham smoking studies were conducted in a randomized order. Compared with sham smoking, acute smoking caused increases in heart rate (smoking, 9.3 ± 4.1 beats/min; sham, -1.3 ± 3.0 beats/min; P < 0.001) and systolic blood pressure (smoking, 6.3 ± 8.8 mmHg; sham, 0.8 ± 4.4 mmHg; P < 0.05); decreases in absolute (smoking, -4.9 ± 6.9 per mm2; sham, 0.8 ± 2.1 per mm2; P = 0.01) and relative (smoking, -13.8 ± 21.4%; sham, 1.9 ± 6.9%; P = 0.02) capillary recruitment during peak reactive hyperaemia; and decreases in absolute [smoking, -62.4 ± 47.7 perfusion units (PU); sham, -30.8 ± 32.6 PU; P = 0.04] and relative (smoking, -147 ± 163%; sham, 32 ± 225%; P = 0.07) vasodilatation caused by acetylcholine. Absolute (smoking, -31.6 ± 58.5 PU; sham, -8.4 ± 44.0 PU; P = 0.3) and relative (smoking, -50.2 ± 219.0%; sham, -17.1 ± 139%; P = 0.7) vasodilatation caused by sodium nitroprusside were not affected. Thus acute smoking is associated with impaired capillary recruitment during peak reactive hyperaemia and impaired microvascular endothelium-dependent vasodilatation. These findings may explain the increased blood pressure and decreased insulin sensitivity that have been observed after acute smoking.
AB - An effect on microvascular function has been proposed as a possible mechanism explaining the association of acute smoking with increased blood pressure and decreased insulin sensitivity. However, the effects of smoking on microvascular function have not been studied. We have investigated the acute effects of smoking on microvascular function in 12 healthy smokers. Before and after smoking a cigarette, we measured heart rate, blood pressure and capillary recruitment during peak reactive hyperaemia. We also measured endothelium-dependent and endothelium-independent vasodilatation of the skin microcirculation with iontophoresis of acetylcholine and sodium nitroprusside respectively combined with laser Doppler fluxmetry. To exclude non-specific changes, a control study with sham smoking was performed. The smoking and sham smoking studies were conducted in a randomized order. Compared with sham smoking, acute smoking caused increases in heart rate (smoking, 9.3 ± 4.1 beats/min; sham, -1.3 ± 3.0 beats/min; P < 0.001) and systolic blood pressure (smoking, 6.3 ± 8.8 mmHg; sham, 0.8 ± 4.4 mmHg; P < 0.05); decreases in absolute (smoking, -4.9 ± 6.9 per mm2; sham, 0.8 ± 2.1 per mm2; P = 0.01) and relative (smoking, -13.8 ± 21.4%; sham, 1.9 ± 6.9%; P = 0.02) capillary recruitment during peak reactive hyperaemia; and decreases in absolute [smoking, -62.4 ± 47.7 perfusion units (PU); sham, -30.8 ± 32.6 PU; P = 0.04] and relative (smoking, -147 ± 163%; sham, 32 ± 225%; P = 0.07) vasodilatation caused by acetylcholine. Absolute (smoking, -31.6 ± 58.5 PU; sham, -8.4 ± 44.0 PU; P = 0.3) and relative (smoking, -50.2 ± 219.0%; sham, -17.1 ± 139%; P = 0.7) vasodilatation caused by sodium nitroprusside were not affected. Thus acute smoking is associated with impaired capillary recruitment during peak reactive hyperaemia and impaired microvascular endothelium-dependent vasodilatation. These findings may explain the increased blood pressure and decreased insulin sensitivity that have been observed after acute smoking.
KW - Endothelium
KW - Iontophoresis
KW - Laser Doppler
KW - Smoking
UR - http://www.scopus.com/inward/record.url?scp=0037336539&partnerID=8YFLogxK
U2 - https://doi.org/10.1042/CS20020318
DO - https://doi.org/10.1042/CS20020318
M3 - Article
C2 - 12605581
SN - 0143-5221
VL - 104
SP - 247
EP - 252
JO - Clinical science
JF - Clinical science
IS - 3
ER -