Lynell C. Collins

Smoking multiple high- versus low-nicotine cigarettes: Impact on resting energy expenditure

The thermic effect of smoking multiple cigarettes varying substantially in nicotine yield was investigated. Three treatments were imposed: nonsmoking at baseline, smoking six low-nicotine (0.8 mg nicotine) cigarettes (LOW), and smoking six high-nicotine (1.74 mg nicotine) cigarettes (HIGH). An initial increase of 6.8% in resting energy expenditure (REE) above baseline REE occurred after consumption of two consecutive cigarettes for both the HIGH and LOW treatments. With consumption of more cigarettes, the peak increase for the HIGH treatment was 9.3%, significantly greater than the peak of 5.9% for the LOW. Averaged over 2 hours, the HIGH treatment significantly increased REE by 6.9% and the LOW treatment significantly increased REE by 5.2%. Expired carbon monoxide (CO) measurements indicated that LOW cigarettes were smoked more aggressively than HIGH cigarettes. It was concluded that, initially, the nicotine yield of cigarettes is not an important influence on the thermic effect of smoking. But over a longer period and after multiple cigarettes, the nicotine yield may become an important influential factor.

The effect of smoking on energy expenditure and plasma catecholamine and nicotine levels during light physical activity

A number of studies have found that cigarette smoking causes an acute increase in resting energy expenditure, but the effect on energy expenditure during light physical activity is less clear. Since both smoking and activity have been shown to increase plasma catecholamines, these could produce additive effects on energy expenditure when smoking during light physical activity. In this study, the impact of cigarette smoking on energy expenditure, cardiovascular function, plasma nicotine and plasma catecholamine levels was determined in adult male subjects at rest and while engaged in light physical activity. Smoking at rest resulted in a 3.6% increase in energy expenditure above the resting baseline; whereas the increase in energy expenditure caused by smoking during light physical activity (compared with the light physical activity baseline) was 6.3%. This increase during light physical activity was significantly greater than the increase observed at rest (p < 0.025). As expected, plasma nicotine increased with smoking during both rest and light physical activity. An increase in plasma nicotine was associated with smoking during light physical activity. When this increase was adjusted as a covariate, the difference in smoking-related energy expenditure between light physical activity and rest disappeared, suggesting nicotine accounts for the effect. Plasma epinephrine and norepinephrine levels increased with smoking and showed a significantly greater increase during light physical activity compared to rest. Cigarette smoking caused a significantly greater increase in heart rate during light physical activity than it did while at rest, but there was no significant effect of smoking on mean blood pressure. It was concluded that there is enhanced energy expenditure associated with cigarette smoking during light physical activity when compared with smoking at rest which could be due in part to smoking-induced increases in circulating plasma catecholamines and perhaps nicotine.

Direct Effects of Meconium on Rat Tracheal Smooth Muscle Tension in Vitro

Increased airway resistance is a component of the meconium aspiration syndrome. Experiments were done to determine whether meconium can have a direct affect on tracheal smooth muscle tension. Tracheal segments (4-5 mm long) were isolated from male Sprague-Dawley rats and suspended in organ baths with physiologic salt solution at 37 °C gassed with 95% O2-5% CO2. Each segment was attached to a fixed glass rod on one side and to a force displacement transducer on the other side to measure transverse tension. The segments were stretched to 1.5 g of tension and equilibrated for 2-5 h. Human meconium was diluted in physiologic salt solution (20 g/100 mL) and filtered through gauze. Tension was generated in the segments by adding acetylcholine (10-6 M) to the tissue bath. Addition of meconium to the organ bath (0.1-5 mg/mL) caused tracheal smooth muscle relaxation in 44% of tracheal segments tested. Contraction occurred in 8% of tested segments, but only at the intermediate and low doses. The amount of relaxation increased significantly in a concentration-dependent manner. These responses were not affected by pretreating segments with indomethacin, removing the tracheal epithelium, using KCl to generate tone, or by heating meconium above 60 °C for 1 h. Addition of oleic acid to the organ bath (3.5 × 10-6 to 3.5 × 10-4 M) caused concentration-dependent tracheal smooth muscle responses (with relaxation predominating at 3.5 × 10-4 M and contraction predominating at 3.5 × 10-6 M). These results suggest that meconium can cause tracheal smooth muscle relaxation by a mechanism that does not appear to be mediated by cyclooxygenase products, by the tracheal epithelium, or a protein. The direct action of meconium on tracheal smooth muscle, which may in part be mediated by a fatty acid, does not appear to contribute significantly to the increased airway tone associated with the meconium aspiration syndrome.