Structural and Functional Alteration of Blood Vessels Caused by Cigarette Smoking: An Overview of Molecular Mechanisms

Abstract

Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Most clinical and experimental investigations of the pathophysiology of cigarette smoking have studied the effects of smoke as a whole, while a few studies focused on specific components of cigarette smoke, e.g. nicotine and carbon monoxide, which are only 2 of the more than 4,000 different chemicals present in cigarette smoke. The findings point to some discrepancies when the effects of whole smoke are compared to nicotine alone, while there is almost uniform agreement that both active and passive smoking have detrimental effects on the cardiovascular system, although a milder effect was suggested for the latter. This review focuses on findings from clinical and experimental studies on the vascular effects of active and passive cigarette smoking and nicotine exposure. The findings are discussed in terms of tissue (conduit vs. resistance arteries and veins), species, age, gender and dosage. Although the exact pathophysiology of cigarette smoking has not been unveiled, cigarette smoking causes injury to the vascular endothelium, produces superoxide anions, reduces production and bioavailability of nitric oxide (NO), increases production and release of endothelin, causes endothelial dysfunction, thrombosis, atherosclerosis, infarction, coronary artery disease (CAD), stroke and death.

Smoking is a risk factor of organ/space surgical site infection in orthopaedic surgery with implant materials

“…Nicotine, nitric oxide, and carbon monoxide directly alter the wound healing process [19,20]. Smoking causes endothelial dysfunction, inflammation, and progression of atherothrombotic disease.…”

The effect of smoking on arterial stiffness

“…Acute and chronic smoking has been shown to induce oxidative stress, altering vascular tone and increasing arterial stiffness. 4,84 Smoking increases the production of reactive oxygen species, which decreases the activity of nitric oxide synthase (NOS), inhibiting nitric oxide (NO) production by the endothelium. 85,86 Platelet-derived NO production also decreases contributing to a hypercoagulable state.…”

Thromboembolic injury and systemic toxicity induced by nicotine in mice

“…The principal sources of nicotine exposure are through the use of tobacco, nicotine containing gum, and nicotine replacement therapies (Yildiz et al 1998). Nicotine is known to have disparaging effects on the cardiopulmonary system which includes lung damage, acute cardiac syndrome, disturbance in the platelet contents and its aggregation, renal circulatory changes, the alteration of the liver functions (Hanna 2006) and is most widely associated with cancer (Bernhard et al 2003;Rahman and Laher 2007). Nicotine plays major role in increasing the blood pressure (Lindenblatt et al 2007) and the atherosclerosis (Lee and Cooke 2011).…”