The Effect of Nicotine on Endothelial Cells of Rat Aorta

Park, Jang Sang; Kim, Joong Yeon; Choi, Hae Kwon; Kim, Seung Nam; Koh, Yong Bok

Abstract

Many studies over the past few years have suggested that cigarette smoking appears to be a risk factor for disease of the cardiovascular system. Smoking has been associated with an increase in arterial thrombosis, ischemic heart disease, myocardial infarction, occlusive peripheral arterial disease, high cholesterol, and hypertension. The increased occurrence of atherosclerotic lesions in autopsied vessels from smokers has also been reported. Recent studies have shown that nicotine has a desquamating effect on endothelial cells and repeated endothelial cell injury has been suggested as an initiating factor in thrombosis and atherosclerosis. This study was conducted to define the effects of chronic oral nicotine consumption on the morphologic characteristics of rat aortic endothelial cells and their distribution. In these experiments, rats of Wistar strain, weighing 250~300 gm, were divided into: normal control group(n=12), acute nicotine group(n=12, 5 mg/kg/day nicotine for 1 week), chronic nicotine group(n=12, 5mg/kg/day nicotine for 10 weeks), cessation group(n=12). Nicotine group were fed a stock diet and administered daily doses of nicotine(5mg/kg/day) in their drinking water. From previous human and animal studies on smoking and oral nicotine consumption, it was estimated that each rabbit consumed about as much nicotine per as a personal smoking 2~4 packs of cigaretts per day. The type of pathologic damage included endothelial cell separation, partial loss of endothelial cell, crater, exposed basement membrane, exposed fibrillar collagen. The damaged endothelial cells among the 100 cells were counted in the scanning electron microscope and the extend of damage was expressed on the basis of percent. The results were as follows: 1) In normal control group, well-preserved endothelial lining with cobble-stone appearance was seen. 2) No significant endothelial cell damage was showed in acute nicotine group. 3) Partial erosion of endothelial lining, intercellular separation and exposure of underlying subendothelial components were examed with 56+/-1.57% of cell damage in chronic group. 4) No significant endothelial disruption or detachment was seen with nomal lining of in control group and acute group with 4.1+/-0.19% of damaged cell respectively. The aorta segments that were treated with nicotine for 10 weeks showed significantily higher degree of endothelial cell damage then there treated for only 1 week. And cessation of nicotine administration didn't decreased the endothelial cell injury. This study indicates that nicotine administered orally to rats, has a demonstrable in vivo morphologic injury effect on endothelial cells in the aorta.