Acute influence of cigarette smoke in platelets, catecholamines and neurophysins in the normal conditions of daily life.
Cigarette smoking is firmly linked to the occurrence of acute coronary events. In twenty-two healthy volunteers in normal conditions of daily life we studied the acute influence of smoking on the following parameters: beta-thromboglobulin, thromboxane B2, epinephrine, norepinephrine, estrogen-stimulated neurophysin, and nicotine-stimulated-neurophysin. Our results show that in our population and following our protocol, smoking did not induce platelet activation, thromboxane formation, catecholamine release or estrogen-stimulated-neurophysin secretion. However, smoking did provoke a significant increase of nicotine-stimulated-neurophysin (p less than 0.05) which reflects vasopressin increase and which might explain the high incidence of ischaemic accidents in cigarette smoking via the vasoactive properties of vasopressin.
D000293:Adolescent; D000328:Adult; D001792:Blood Platelets / Q000187:drug effects*; D004837:Epinephrine / Q000097:blood*; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009481:Neurophysins / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood*; D012907:Smoking; D013268:Stimulation, Chemical; D013929:Thromboxane B2 / Q000097:blood; D001620:beta-Thromboglobulin / Q000097:blood
D004967:Estrogens; D009481:Neurophysins; D001620:beta-Thromboglobulin; D013929:Thromboxane B2; D009638:Norepinephrine; D004837:Epinephrine