Exposure to prolonged puffing can perk up levels of a stress hormone in the heart that can potentially reshape the left ventricle, according to new research.
In a Chicago University (Illinois) [CUI] study using rats as animal model, a five-week exposure to cigarette smoke was associated with the activation of enzymes called mitogen-activated protein kinases that govern cell growth and survival in heart muscle.
Activation of these enzymes may be a key event in cigarette smoke-induced heart injury, said Mariann Piano, professor of bio-behavioural health science in the CUI College of Nursing, who led the study. “Cigarette smoke contains more than 4,000 different chemicals, one of which is nicotine,” Piano said. “However, the effect of nicotine on the initiation and progression of cigarette smoke-mediated cardiovascular events remains controversial.”
To date, small clinical trials of nicotine replacement therapies have not shown increased cardiovascular risk, even in patients with cardiovascular disease, Piano said. This suggested the need to study cigarette smoke as a whole, according to a Chicago release. In the new study, rats were exposed either to cigarette smoke or to normal room air. After five weeks, the animals were examined by echocardiography. Heart tissue was examined under the microscope and by Western blot analysis, used to detect specific proteins in tissue samples. The results showed exposure to cigarette smoke was associated with significant changes in the shape of the left ventricle, the heart’s main pumping chamber, and an increase in the levels of the activated forms of the enzymes in the heart muscle. Researchers also found increased levels of norepinephrine, a hormone released when a stressful event causes any of a host of physiological changes, in urine samples taken from the animals.