Study On Effect Of The Nicotine On Rat Cardioelectric And Other Physiological Characteristics

Base on the animal test,Studies on nicotine have transfered from its negatively effect to exploitation and utilization in biology medicine.Studies on effects and mechanism of action of Nicotine in biology medicine also developed.Controversy on Nicotine can or not becoming medecines of healing disease became more and more violent.The newest researchs domestic and international,reviewed the physico-chemical property,Nicotinic choline receptors,effects and mechanism in agriculture and biology medicine of Nicotine.The nicotine has a stage function to the heart rate,first nicotine administration cause a brief decrease followed by a much larger increase.Record the ECG at the nicotine act to rat after,discovering the nicotine can cause a longer QT interval,increaseing the PR interval and T-wave area,with the function likeness of adrenaline or noradrenalin,it was blocked by M-receptor antagonist atropine,indicate nicotine can inducement local release acetylcholine or directness act on muscarinic cholinoreceptor was control by parasympathetic. AD is internal hormone effect onαandβreceptor,NA isβreceptor selectivity depressant,For study this effection,we to utilize rat ECG experimentize.Nicotinic acetylcholine receptors are pentameric,typically composed of a andβ.To investigate the receptor subty,pes are active in the heart,initiated a series of experiments with rat preparation.Nicotine administration(100μmol·L^-1) caused a brief decrease(-7±2%) followed by a much larger increase(17±5%) in heart rate that slowly returned to baseline within 10 to 15 min.The nicotine-induced decrease in heart rate could be abolished by an a₇-specific antagonist,a-hungarotoxin(100nmol·L^-1).In contrast,the nicotine-induced increase in heart rate persisted in the presence of a-bungarotoxin.To investigate which subunits may contribute to the nicotine-induced increase in heart rate,repeated the experiments with cytisine,an agonist at nAChRs that containβ₄ subunits.The cytisine results were similar to those obtained with nicotine,thereby suggesting that the nAChRs on sympathetic nerve terminals in the heart probably containβ₄ subunits.Thus,the results of this study;show that pharmacologically distinct nAChRs are responsible for the differential effects of nicotine on heart rate.More specifically,our results suggest that a₇ subunits participate in the initial nicotine-induced heart rate decrease,where asβ₄ subunits help to mediate the subsequent nicotine-induced rise in heart rate.Rat long-term toxicity test to showed that high dose to display body,weight descend,blood biochemistry index TG and CK increase,liver weight descend,histopathology to originated compensation or straight effection to organ.but nuable definite now.