On the mechanism of barium induced diastolic depolarisation in isolated ventricular myocytes

Barium can induce spontaneous activity in cardiac non-pacemaker cells. The mechanism of barium induced diastolic depolarisation was studied in isolated ventricular myocytes, using a microelectrode technique. Barium (0.05-0.2 mmol.litre-1) decreased resting potential and caused the membrane potential at the end of the action potential to undershoot the diminished resting value temporarily, thereby inducing diastolic depolarisation. Resting membrane resistance was increased by Ba but at the end of phase 3 repolarisation the resistance temporarily decreased below its steady state diastolic value. In presence of Ba, hyperpolarisation abolished or reversed diastolic depolarisation. At the end of phase 3 repolarisation, membrane resistance was decreased, whether diastolic depolarisation was present, absent or reversed. A high [K]o (15.4 mmol.litre-1) decreased Ba effects on action potential, membrane resistance and diastolic depolarisation. Caesium decreased the Ba induced diastolic depolarisation and the associated increase in membrane resistance, but had little effect on spontaneous activity at depolarised levels. Barium induced an oscillatory potential, with increased membrane resistance. Noradrenaline plus low [Ba]o, and high [Ba]o alone (1-5 mmol.litre-1), can induce spontaneous activity. Thus, in myocardial cells barium induces diastolic depolarisation at polarised levels by a voltage and time dependent block of potassium conductance, which is modulated by action potential voltage changes. However, as [Ba]o is increased, spontaneous activity at a depolarised level may be related to the decay of potassium currents and to oscillatory potentials.     

筛检对肝癌死亡率影响的研究

5581名HBsAg阳性的男性随机分入周期性筛检组(A组,3712人)及对照组(B组,1869人)。A组(19155.4人年)共发生肝癌257例,B组(9785.5人年)为117例,两组的肝癌发生率分别为1342/10万与1196/10万;两组肝癌死亡分别为218与109例,肝癌死亡率分别为1138/10万与1114/10万。两组中Ⅰ期肝癌病例分别为29.6％与6.0％,差异有非常显著性意义。1、3、5年相对生存率A组为23.7％、7.0％、4.0％,B组为9.7％、4.0％、4.1％。用Poisson回归模型拟合显示,在调正年龄、初筛AFP及入列年份后,筛检对于肝癌的相对危险度为0.83,95％CI为0.68～1.03,有较弱的“保护”作用,Cox回归模型拟合结果显示当临床分期未引入模型时,筛检对于肝癌有显著的“保护”作用:危险率为0.6617,95％CI为0.5234～0.8365;而模型经调整后,危险率即接近“1”,95％CI为0.74～1.26。