Smoking can increase gastric acid secretion, which is generally 965438 0.5% higher than that of non-smokers, and can inhibit the secretion of sodium bicarbonate by pancreas, thus increasing duodenal acid load and inducing ulcer.
Nicotine in tobacco can reduce the tension of pyloric sphincter, make bile easy to reflux, thus weaken the defense factors of gastric and duodenal mucosa, promote chronic inflammation and ulcer, and delay the healing of original ulcer. In addition, smoking can reduce the tension of lower esophageal sphincter and easily cause reflux esophagitis.
Extended data:
Main danger
① Carcinogenesis
Although smokers don't accept it, it is universally acknowledged that smoking causes cancer. Epidemiological investigation shows that smoking is one of the important pathogenic factors of lung cancer, especially squamous cell carcinoma and small cell undifferentiated carcinoma.
The risk of lung cancer of smokers is 13 times that of non-smokers. If you smoke more than 35 cigarettes a day, your risk is 45 times that of non-smokers. The mortality rate of lung cancer in smokers is 10~ 13 times higher than that in non-smokers. About 85% of lung cancer deaths are caused by smoking. If smokers are exposed to chemical carcinogens such as asbestos, nickel, uranium and arsenic at the same time,
PAHs in tobacco smoke are cytotoxic and mutagenic only after being metabolized by PAH hydroxylase, and the concentration of this hydroxylase in smokers is higher than that in non-smokers.
Smoking will reduce the activity of natural killer cells, thus weakening the body's function of monitoring, killing and clearing tumor cells, which further explains that smoking is a high risk factor for many cancers. The incidence of laryngeal cancer and bladder cancer in smokers is ten times higher than that in non-smokers, which may be related to β -naphthylamine in smoke.
In addition, smoking is also related to the occurrence of lip cancer, tongue cancer, oral cancer, esophageal cancer, gastric cancer, colon cancer, pancreatic cancer, renal cancer and cervical cancer. Clinical research and animal experiments show that carcinogens in smoke can also affect the fetus through the placenta, leading to a significant increase in the incidence of cancer in its offspring.
② Influence on cardiovascular and cerebrovascular diseases.
Many studies believe that smoking is the main risk factor of many cardiovascular and cerebrovascular diseases, and the incidence of coronary heart disease, hypertension, cerebrovascular disease and peripheral vascular disease of smokers has increased significantly.
Statistics show that 75% of patients with coronary heart disease and hypertension have a history of smoking. The incidence of coronary heart disease in smokers is 3.5 times higher than that in non-smokers, the mortality of coronary heart disease is 6 times higher, and the incidence of myocardial infarction is 2~6 times higher. Pathological anatomy also found that coronary atherosclerosis in the former was more extensive and serious than that in the latter.
Hypertension, high cholesterol and the incidence of coronary heart disease in smokers increased by 9~ 12 times.
30~40% of cardiovascular deaths are caused by smoking, and the increase of mortality is directly proportional to the amount of smoking. Nicotine and carbon monoxide in smoking are considered to be the main harmful factors causing coronary atherosclerosis, but the exact mechanism is not fully understood. Most scholars believe that blood lipid changes, platelet function and abnormal hemorheology play an important role.
High density lipoprotein cholesterol (HDL-C) can stimulate vascular endothelial cells to produce prostacyclin (PGI2), which is the most effective substance to dilate blood vessels and inhibit platelet aggregation.
Smoking can damage vascular endothelial cells, decrease serum HDL-C, increase cholesterol and decrease PGI2-2 level, thus causing peripheral blood vessels and coronary arteries to contract, wall to thicken, lumen to narrow, blood flow to slow down, resulting in myocardial hypoxia. Nicotine can promote platelet aggregation.
Carbon monoxide in smoke combines with hemoglobin to form carboxyhemoglobin, which affects the oxygen carrying capacity of red blood cells and causes tissue hypoxia, thus inducing coronary artery spasm. Due to tissue hypoxia, compensatory erythrocytosis and blood viscosity increase. In addition, smoking can increase the level of plasma fibrinogen, leading to dysfunction of coagulation system.
Smoking can also affect the metabolism of arachidonic acid, reduce PGI2 _ 2 production and increase thromboxane A _ 2 relatively, thus causing vasoconstriction and increasing platelet aggregation. All of the above may promote the occurrence and development of coronary heart disease. Due to myocardial hypoxia, myocardial stress increases and ventricular fibrillation threshold decreases, so patients with coronary heart disease who smoke are more prone to arrhythmia and the risk of sudden death increases.
It is reported that the risk of stroke of smokers is 2~3.5 times that of non-smokers. If smoking and hypertension coexist, the risk of stroke will increase nearly 20 times. In addition, smokers are prone to arteriosclerosis obliterans and thromboangiitis obliterans. Smoking will lead to chronic obstructive pulmonary disease, and eventually lead to pulmonary heart disease.
③ Influence on respiratory tract
Smoking is one of the main causes of chronic bronchitis, emphysema and chronic airway obstruction. Experimental research shows that long-term smoking can damage and shorten the cilia of bronchial mucosa and affect the cilia removal function.
In addition, submucosal gland hyperplasia, hypertrophy, increased mucus secretion, composition has also changed, easy to block bronchioles. In dog experiments, exposure to a large amount of smoke can cause changes in emphysema.
The number of macrophages (AM), neutrophils (PMN) and elastase in the lower respiratory tract of smokers is significantly higher than that of non-smokers. The mechanism may be due to the stimulation of smoke particles and harmful gases, which activated the mononuclear phagocyte system in the lower respiratory tract. Activated AM not only releases elastase, but also releases PMN chemokines, which makes PMN transfer from capillaries to lungs.
Activated AM also releases macrophage growth factor to attract fibroblasts. However, PMN releases a large number of toxic oxygen free radicals and proteolytic enzymes, including elastase and collagenase, which act on elastin, mucin, basement membrane and collagen fibers of the lung, thus leading to the destruction of alveolar septa and interstitial fibrosis.
It is reported that there were nearly130 thousand COPD patients in the United States during 1986, and more than 90 thousand people died in 199 1 year. Smoking is the main reason. The probability of smokers suffering from chronic bronchitis is 2 ~ 4 times higher than that of non-smokers, and it is directly proportional to the amount of smoking and the number of years of smoking. Patients often have chronic cough, expectoration and dyspnea during activities.
Pulmonary function examination showed airway obstruction, decreased lung compliance, ventilation function and diffusion function, and decreased arterial oxygen partial pressure. Even young asymptomatic smokers have slight pulmonary dysfunction. Chronic obstructive pulmonary disease is prone to spontaneous pneumothorax. Smokers often suffer from chronic pharyngitis and vocal cord inflammation.
④ Influence on digestive tract
Smoking can increase gastric acid secretion, which is generally 965438 0.5% higher than that of non-smokers, and can inhibit the secretion of sodium bicarbonate by pancreas, thus increasing duodenal acid load and inducing ulcer.
Nicotine in tobacco can reduce the tension of pyloric sphincter, make bile easy to reflux, thus weaken the defense factors of gastric and duodenal mucosa, promote chronic inflammation and ulcer, and delay the healing of original ulcer. In addition, smoking can reduce the tension of lower esophageal sphincter and easily cause reflux esophagitis.
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