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Cigarette smoking is hazardous for various tissues in human. The cigarette smoke inhalation has been proved to delay bone healing. However, no previous study demonstrates the smoking effect on bony microcirculation. In this study, we investigated the effect of cigarette smoking on tibial vascular endothelium and blood flow by using the bone chamber model.

Eighteen adult New Zealand rabbits were divided into 3 groups. Group 1: Control, Group 2: 1 week smoking, and Group 3: 6 weeks smoking. All these rabbits were then anesthetized, and their nutrient arteries of tibia were identified and cannulated. We put the tibia into bone chamber after cannulation, perfused with Krebs-Ringer solution (phase 1), and then compared the effect of vasospasm by norepinephrine dose-response curve (NEDRC). Acetylcholine (phase 2) and L-NMMA (phase 3) were also perfused and the NEDRC recorded. Acetylcholine can stimulate the release of nitric oxide and lower the NEDRC. L-NMMA inhibits NO synthesis in vascular endothelium, and hence results in vasoconstriction under various stimuli. Data collection and statistic processing were performed by ANOVA analysis.

The NEDRC data in Group 1 (control) was set to be 100%. In phase 1 study, our results showed that 1 week cigarette smoking significantly increased NEDRC in Group 2 (142.5%, p<0.01). However, 6 weeks smoking strikingly boosted the response of NEDRC in Group 3 (226.5%, p<0.01). In phase 2 study, Group 2 tibia showed the NEDRC under acetylcholine perfusion to be without any difference in comparison with Group 1 (p>0.05). Nevertheless, Group 3 tibia showed significant vasospasm even under acetylcholine perfusion. In phase 3 study, L-NMMA perfused data revealed that; Group 3 tibia had the highest NEDRC, i.e. the most severe vasospasm.

Based on our study, both short-term and long-term cigarette smoking are hazardous to the bony vascular endothelium. The nitric oxide production significantly attenuated in Group 2 and 3 tibia. However, the adverse effect of smoking seems reversible in short-term (Group 2). Long-term smoking (Group 3) causes irreversible damage to vascular endothelium and muscarinic receptor.

Cigarette smoking is regarded as a risk factor for developing complications in fracture healing. To determine whether nicotine would retard fracture healing in the rat, 25 rats were divided into two groups and given nicotine or saline subcutaneously at a dose of 2 mg/kg a day, for four weeks. Then their right forelimbs were broken. The rats were killed and histopathologic sections of the radius and ulna were examined and graded at the 7th and 21st days after fractures. Nicotine or saline treatment continued throughout the experiment. Median fracture healing score was found to be 0 (min. 0 - max. 1) in nicotine-treated rats, and 1 (min. 0 - max. 2) in controls, at the 7th day. At the 21st day, the median scores were 2 (min. 1 - max. 3), and 3 (min. 2 - max. 3) in experimental and control groups, respectively. Scores were significantly decreased in nicotine-treated rats both at the 7th and 21st days (p = 0.0465 and p = 0.0175, respectively). We suppose that nicotine impaired fracture healing in the rat forearm model possibly by diminishing nutritional blood flow via vasoconstriction and by its direct effect on osteogenesis.

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