Sørensen Lars Tue, Nielsen Henning Bay, Kharazmi Arsalan, Gottrup Finn
Copenhagen Wound Healing Center, the Department of Surgical Gastroenterology, Bispebjerg Hospital, University of Copenhagen, DK-2400 Copenhagen, Denmark.
Surgery. 2004 Nov;136(5):1047-53. doi: 10.1016/j.surg.2004.04.001.
Smoking is associated with surgical wound infections, impaired wound healing, and tissue-destructive disorders. The mechanisms are largely unknown, but changes in the function and activity of inflammatory cells may be involved.
Seventy healthy volunteers (54 smokers and 16 never smokers) were included. The smokers were studied while they smoked and after 20 days of abstinence. After the first 10 days of abstinence, they were randomized to double-blind treatment with transdermal nicotine patch 25 mg per day or placebo. Venous blood neutrophils and monocytes were sampled and isolated. In 22 randomly selected smokers and in all never smokers, the oxidative burst and chemotaxis were determined by a chemiluminescence response assay and a modified Boyden chamber technique, respectively. Stimulants were opsonized zymosan, formyl-Met-Leu-Phe, and zymosan-activated serum.
The neutrophil and monocyte oxidative burst was 50% and 68% lower, respectively, in smokers compared to never smokers (P < .05). Neutrophil chemotaxis was 93% higher in smokers (P < .05). Monocyte chemotaxis was lower in smokers compared to never smokers (P < .05). After 20 days of abstinence, neutrophil oxidative burst increased to the level of never smokers (P < .05); monocyte oxidative burst increased by 50% (P < .05). Chemotaxis was only marginally affected. The changes induced by abstinence were less pronounced in the transdermal nicotine patch group compared to the placebo group.
Smoking attenuates the oxidative burst of inflammatory cells and increases chemotaxis. Three weeks of abstinence normalize the oxidative burst, but affect chemotaxis only marginally.
吸烟与手术伤口感染、伤口愈合受损及组织破坏性疾病相关。其机制大多未知，但可能涉及炎症细胞功能和活性的改变。
纳入70名健康志愿者（54名吸烟者和16名从不吸烟者）。对吸烟者在吸烟时及戒烟20天后进行研究。在戒烟的前10天之后，他们被随机分为双盲治疗组，分别接受每天25毫克的经皮尼古丁贴片或安慰剂治疗。采集并分离静脉血中的中性粒细胞和单核细胞。在22名随机选择的吸烟者和所有从不吸烟者中，分别通过化学发光反应测定法和改良的博伊登小室技术测定氧化爆发和趋化性。刺激物为调理酵母聚糖、甲酰 - 甲硫 - 亮 - 苯丙氨酸和酵母聚糖激活血清。
与从不吸烟者相比，吸烟者的中性粒细胞和单核细胞氧化爆发分别降低了50%和68%（P <.05）。吸烟者的中性粒细胞趋化性高93%（P <.05）。吸烟者的单核细胞趋化性低于从不吸烟者（P <.05）。戒烟20天后，中性粒细胞氧化爆发增加到从不吸烟者的水平（P <.05）；单核细胞氧化爆发增加了50%（P <.05）。趋化性仅受到轻微影响。与安慰剂组相比，经皮尼古丁贴片组中戒烟引起的变化不太明显。
吸烟会减弱炎症细胞的氧化爆发并增加趋化性。三周的戒烟可使氧化爆发恢复正常，但对趋化性的影响很小。
