Publication Date:
2013-03-03
Description:
Cigarette smoking attenuates acetylcholine (ACh)-induced cutaneous vasodilation in humans, but the underlying mechanisms are unknown. We tested the hypothesis that smokers have impaired nitric oxide (NO)- and cyclooxygenase (COX)-dependent cutaneous vasodilation to ACh infusion. Twelve young smokers, who have smoked more than 5.2 ± 0.7 yr with an average daily consumption of 11.4 ± 1.2 cigarettes, and 12 nonsmokers were tested. Age, body mass index, and resting mean arterial pressure were similar between the groups. Cutaneous vascular conductance (CVC) was evaluated as laser-Doppler flux divided by mean arterial pressure, normalized to maximal CVC (local heating to 43.0°C plus sodium nitroprusside administration). We evaluated the increase in CVC from baseline to peak (CVC peak ) and area under the curve of CVC (CVC AUC ) during a bolus infusion (1 min) of 137.5 μM ACh at four intradermal microdialysis sites: 1 ) Ringer (control), 2 ) 10 mM N G -nitro- l -arginine methyl ester ( l -NAME; NO synthase inhibitor), 3 ) 10 mM ketorolac (COX inhibitor), and 4 ) combination of l -NAME + ketorolac. CVC peak and CVC AUC at the Ringer site in nonsmokers were greater than in smokers (CVC peak , 42.9 ± 5.1 vs. 22.3 ± 3.5% max , P 〈 0.05; and CVC AUC , 8,085 ± 1,055 vs. 3,145 ± 539% max ·s, P 〈 0.05). In nonsmokers, CVC peak and CVC AUC at the l -NAME site were lower than the Ringer site (CVC peak , 29.5 ± 6.2% max , P 〈 0.05; and CVC AUC , 5,377 ± 1,109% max ·s, P 〈 0.05), but in smokers, there were no differences between the Ringer and l -NAME sites (CVC peak , 16.8 ± 4.3% max , P = 0.11; and CVC AUC , 2,679 ± 785% max ·s, P = 0.30). CVC peak and CVC AUC were reduced with ketorolac in nonsmokers (CVC peak , 13.3 ± 3.6% max , P 〈 0.05; and CVC AUC , 1,967 ± 527% max ·s, P 〈 0.05) and smokers (CVC peak , 7.8 ± 1.8% max , P 〈 0.05; and CVC AUC , 1,246 ± 305% max ·s, P 〈 0.05) and at the combination site in nonsmokers (CVC peak , 15.9 ± 3.1% max , P 〈 0.05; and CVC AUC , 2,660 ± 512% max ·s, P 〈 0.05) and smokers (CVC peak , 11.5 ± 2.6% max , P 〈 0.05; and CVC AUC , 1,693 ± 409% max ·s, P 〈 0.05), but the magnitudes were greater in nonsmokers ( P 〈 0.05). These results suggest that impaired ACh-induced skin vasodilation in young smokers is related to diminished NO- and COX-dependent vasodilation.
Print ISSN:
0363-6135
Electronic ISSN:
1522-1539
Topics:
Medicine
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