Physiological response to smoking, are all, except:
Decreased carboxyhemoglobin Physiological effects of smoking The extent of the effects of smoking is related to the number of cigarettes smoked, smoking duration, the amount and type of smoke inhaled. Nicotine in tobacco and smoke stimulates the adrenal medulla, increasing plasma adrenaline and urinary catecholamines and their metabolites. Plasma glucose concentration is enhanced within min after the sta of smoking, often persisting for an hour or so after smoking ceases. Plasma insulin rises about an hour after smoking. Plasma growth hormone concentration may increase tenfold within 30 min after the smoking of one cigarette. Smoking increases the hea rate of smoker, both at rest and in exercise. There is an associated increase of both cardiac output and systemic blood pressure. These changes can be attributed to nicotine inducing release of the hormone noradrenaline. Cigarette smoking is associated with an increased risk and extent of advanced atherosclerotic vascular disease in peripheral as well as coronary aeries. The likelihood of claudication, amputation, stroke, abdominal aoic aneurysm, and failure of vascular reconstruction is higher in smokers than nonsmokers. Smoking exes its deleterious effects through many interactive mechanisms. Nicotine and carbon monoxide produce acute cardiovascular consequences, including altered myocardial performance, tachycardia, hypeension, and vasoconstriction. Smoking injures blood vessel walls by damaging endothelial cells, thus increasing permeability to lipids and other blood components. Among metabolic and biochemical changes induced by smoking are elevated plasma, free fatty acids, elevated vasopressin, and a thrombogcnic balance of prostacyclin and thromboxane A 2. Chronic smoking is associated with a tendency for increased serum cholesterol, reduced high density lipoprotein, and other lipid effects that contribute to atherosclerosis. Hematological changes from increased erythrocytes, leukocytes, and fibrinogen causes alterations in platelet aggregation and survival that produce thrombosis. Smokers have higher plasma beta-lipoprotein. cholesterol, and triglyceride concentrations than nonsmokers. Smoking increase total red blood cells, carboxyhemoglobin and leukocyes, but decreases blood paial pressure of oxygen in habitual smokers. The hematocrit is increased. Smoking affects the immune response, lowering serum IgA, IgG, and IgM but raising IgE.
Decreased HDL
Increased hematocrit
Increased hea rate and increased catecholamine release
Decreased carboxyhemoglobin