OBJECTIVE: Differential cognition and evaluation of the scientific merit of free radical-induced aging theory in the explanation of aging mechanism.DATA SOURCES: Literatures about free radical-induced aging theory were searched in Medline and Embase by computer from April 1976 to October 2004 with searching words of "free radical, aging, dialectical" and the language of the articles was limited in English, the subjects were the elderly and aging animal.STUDY SELECTION: To select literatures about free radical-induced aging theory for preliminary examines. Quality evaluation mainly examined the authenticity of the data, whether the survey design was rigorous, whether the intervention process was strict, and whether statistical management was reasonable.DATA EXTRACTION: A total of 30 articles about the merit of free radical-induced aging theory in the explanation of aging mechanism were searched, of which 18 experiments were in accorded with the inclusive criteria. In the 12 excluded experiments, 7 articles were the repetitions of same study, and 5 articles were Meta analytic study.DATA SYNTHESIS: Comparative analysis was conducted in the experimental results of aging essence and the prolongation of maximum duration of life explained by free radical-induced aging theory.CONCLUSION: Free radical-induced aging theory has an important biomedical academic merit, but it does not successfully explain the fundamental reason of agingand the essence of aging process.

PURPOSE: To know whether the cardiac function of the patients with heart disease is impaired or improved after long-term taking ?-AR antagonists. METHODS: After giving the rats ?-AR selective antagonist, atenolol, for 12wk, the method of radioligand binding assay and the experiment of isolated left-atrium contractive function were carried out to observe the quantity and distribution of ?-AR, its subtypes, ?-AR, and the change of left - atrium contractive function. RESULTS: After long-term administration of atenolol, there were no any obvious changes in ?-AR, the density of the total ?-AR, ?1-AR, and the proportion of ?2-AR in tota1 amount of ?-AR, but the con centrat ion - response cu rves shi fted l e ftwa rd s si gn ifi cant ly as compared with control group- The PA2 value of isoprotenol(ISO) - induced positive inotropic effect after antagonized by ?1-AR selective antagonist CGP20712A in atenolol group was increased significantly as compared with control group. But the PKB value after antagonized by ICI 118511 showed no obvious difference between two groups. HPLC detection showed that the level of plasma atenolol was 3. 5pmol/L in atenolol group and the leveIs of plasma norepinephrine had no significant difference between two groups. But the level of plasma adrenaline in atenolol group was obviously lower than that in control group. CONCLUSIO- N: The long-term administration of ?l-AR antagonist will cause significant increase of the sensitivity of heart ?-AR, especially ?1-AR to excitant ISO. But the number of ?-AR and its subtypes did not change significantly. Besides, after the long-term administration of ?1-AR antagonist atenolol, the level of plasma adrenaline in rats was much lower than that in control group.