Background
The compounds in cigarette smoke are believed to cause oxidative stress, leading to endothelial dysfunction. Understanding the mechanism of endothelial dysfunction due to cigarette smoke is useful for the development of early and preventive therapy for cardiovascular diseases (CVDs) with smoking risk factors.
Conclusion
Subchronic exposure to cigarette smoke caused a decrease in SOD activity and eNOS levels, but no significant change in MDA levels. This study also indicated that smoking causes IMT thickening and pathological structural changes in the aorta. Another finding indicated that a decrease in eNOS levels could cause an increase in the IMT of the aorta.
Methods
In this experimental study, a posttest-only control group design was used. 20 Wistar rats were divided into two groups: a smoking group (exposed to 40 cigarettes per day for 4 weeks) and a control group. After the exposure, the animals were sacrificed and aortas were removed for measurement of malondialdehyde (MDA), superoxide dismutase (SOD), endothelial nitric oxide synthase (eNOS), intima-media thickness (IMT), and for histological analysis.
Results
Exposure to cigarette smoke caused a significant decrease in SOD activity (24.28 ± 4.90; P = 0.027) and eNOS levels (50.81 ± 4.18; P = 0.014), but no significant effect on the level of MDA (17.08 ± 5.78; P = 0.551). Histological analysis showed an increase in IMT (13.27 ± 2.40; P = 0.000) and disorganization and vacuolation of smooth muscle cells in tunica media after exposure to cigarette smoke. The regression analysis showed a significant negative relationship between the eNOS level and IMT (β = -1.012, P = 0.009).