Aconitine On The Mechanism Of Myocardial Cytotoxicity

Objiective:To research the toxicity mechanism of the aconitine damaging myocardial cell.Methods: reseaching the infection that aconitine of different strength infect the myocardial cell in different time by homogeneous design and MTT; researhing infection of myocardial cell of morphologic resulting from the aconitine of most toxic does in critical time by H.E dyeing and electron microscopetoxicity; Observing infection of the completenes of mycardiac cell membrane , the balance of inner mycardiac cell, energy metabolizing , cell cycle with the methods of cell enzymology ,FCM and nephelometery; to research the toxicity mechanism of the aconitine damaging myocardiac cell.Results: The maximum dose and critical time of aconitine destroying mycardiac cell separatly are 3%,30s,1m and 30m. under the microscope ,the connections among cells reducing ,the space among cells enlarging ,vocuole appering in the cells , the completenes of cell membrane being spoiled , cell organs swelling , cell nucles ;dying red ; nucle chromatin condensing and disappearing , chondriosome swelling and dissolving, ribosome swelling and dissolving , ribosome reputring and dissovling,vocuole appering in the cells , integrality of cytolemma bing demaged, protruding of cytolemma dissappearing ,after AC acting on cells; the degree of destorying have relation to the length of time of AC acting on cells , more long the time is ,more serious the cell are damaged the livingness of LDH ,ACP and the amont of MDA increasing , the livingness of Na⁺-K⁺ATP,SDH and the amount of heptain rdducing ,the ratio of the CAMP/CGMP increasing.Concusions: AC directly damages the chromatin, chondriosome, ribosome, ysosome,membrane ,connction of myocardial cell , toxicity of AC results in the biology membrane damaged, hindrane of energy metabolizing ,nucleic acid damaged ;the toxicity mechanism of the AC is possible that the AC restrains the living of Na⁺-K⁺ATP, which results in the [Na⁺] inner the cell increas and the overloading of the [ca²⁺] inner the cell,which results in the damage of the configuration and action .