Meity Ardiana - Lecturer, Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Airlangga, Surabaya, Indonesia
Budi Pikir - Professor, Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Airlangga, Surabaya, Indonesia
Anwar Santoso - Lecturer, Department of Cardiology, Faculty of Medicine, University of Indonesia; National Cardiovascular Center, Harapan Kita Hospital, Jakarta, Indonesia
Hanestya Hermawan - Resident, Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Airlangga, Surabaya, Indonesia
Makhyan Al-Farabi - Resident, Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Airlangga, Surabaya, Indonesia

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.METHODS: In this experimental study, a posttest-only control group design was used. ۲۰ Wistar rats were divided into two groups: a smoking group (exposed to ۴۰ cigarettes per day for ۴ 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 (۲۴.۲۸ ± ۴.۹۰; P = ۰.۰۲۷) and eNOS levels (۵۰.۸۱ ± ۴.۱۸; P = ۰.۰۱۴), but no significant effect on the level of MDA (۱۷.۰۸ ± ۵.۷۸; P = ۰.۵۵۱). Histological analysis showed an increase in IMT (۱۳.۲۷ ± ۲.۴۰; P = ۰.۰۰۰) 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 = –۱.۰۱۲, P = ۰.۰۰۹).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.

Cigarette Smoke, Vascular Endothelium, Oxidative Stress, Nitric Oxide Synthase