[Effects of prolyl-valine on electrical activities of rat hearts in situ and its antiarrhythmic action (author's transl)].
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Biomedical subjects
T F Liu
Publications and source records attributed to T F Liu.
Effects of TPA on dye transfer and dye leakage in fibroblasts transfected with a connexin 43 mutation at ser368.
In order to investigate the site of active phosphorylation under treatment with TPA, both wild type (WT) fibroblasts and fibroblasts from Cx43-knockout mice transfected with Cx43 mutated at ser368 were used to study the effects of TPA on dye leakage and gap junction assembly. Results showed that in control conditions with or without EGTA, no significant differences in dye leakage were observed between these two kinds of cells. However, under TPA treatment, non-leakage cases in the mutant cells were much less than those in WT cells. In the two types of reaggregated cells, there was a marked difference in the capacity for dye transfer. Dye transfer in WT cells was 4-fold stronger than in mutant cells. While under TPA treatment, the difference between WT and mutant cells was diminished suggesting that ser368 was probably the most important phosphorylation site under treatment with TPA.
Alanine↗
Intracellular lucifer yellow leakage from Novikoff cells in the presence of ATP or low extracellular Ca: evidence for hemi-gap junction channels.
Lucifer Yellow was microinjected into Novikoff hepatoma cells and leakage was investigated under treatment with ATP (5 mM) and EGTA (5 mM) in the culture medium. In control conditions, there was no leakage in single or paired cells, except a few cases which showed very slow leakage (defined as slope < -0.0007/sec). Slow leakage rate (slope > -0.0008 but < -0.009/sec) and quick leakage rate (slope > -0.01) of intracellular dye were not seen. Dye transfer between cell pairs after Lucifer Yellow was injected into one cell was divided into two groups: quick transfer rates (4 cases, slope = -0.151 +0.0032) and slow transfer rates (15 cases, slope = -0.041 +0.0018). Under ATP treatment the intracellular dye leakage was observed in single cells (16 of 31 cases) and in cell pairs (20 of 57 cases). Extracellular low Ca2+ (EGTA treatment) enhanced the dye leakage much more: 30 of 40 cases in single cells and 21 of 36 cases in cell pairs. The leakage rates of intracellular dye under these treatments were similar to the transfer rates of the dye between cell pairs with quick and slow rates. It is suggested that the dye leakage from Novikoff cells under treatment with ATP or low [Ca2+]o shares the same mechanism as dye transfer through gap junctions, suggesting that the hemichannels in the plasma membrane can be opened under certain conditions.
Adenosine Triphosphate↗
Generation of early afterdepolarization in mouse ventricular fibers at long cycle length.
Early afterdepolarization (EAD) was studied in ventricular fibers of mouse heart. EAD could be occasionally induced under long cycle length of superfusion with Tyrode's solution (containing 3.0 or 5.0 mM KCl) at long cycle length. Three types of EAD were found: a second plateau with a prominence, a single triggered burst and a train of triggered bursts. Take-off potential of the first triggered burst or of the prominence varied from -40 to -60 mV. The triggered bursts in the third type often stopped at -35 to -45 mV level forming a very long second plateau before it completely repolarized. Changing abruptly from a long cycle length to a short one lead to a transient EAD induction. It is suggested that EAD in ventricular fiber in mouse heart shared the characteristics of that in atrial fibers, although it was very difficult to induce and was not very reproducible.
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Role of inward and delayed rectifier currents in generation of early afterdepolarization in guinea pig ventricular myocytes under K(+)-free or low K+ superfusion.
Early afterdepolarization (EAD) was studied in isolated ventricular myocytes of guinea pig heart. Under K(+)-free's treatment, most of the myocytes showed hyperpolarization in resting potential and the duration of action potential was prolonged, eventually leading to the appearance of EAD with the second plateau of -76 +/- 3 mV. TTX (10 microM) and verapamil (10 microM) or normal Tyrode's solution abolished the EAD. The background I-V curve showed inward rectifying with a crossover in the level of -80 to -30 mV and the reversal potential shifted from -80 to -120 mV when normal Tyrode's solution was changed to K(+)-free solution. The changes of I-V relationship of inward current IK) were similar to the background ones except without crossover. The delayed rectifier current (IK) was inhibited significantly under K(+)-free treatment. Low K+ (2.7 mM) superfusion was able to induce EAD in only a few cases (4/15). Adding Cs+ (5.0 mM) into low K+ solution, EAD was induced in almost every case. The background I-V curve was inhibited slightly under low K+ superfusion, but was inhibited significantly with a remarkable crossover under low K+ and Cs+ treatment. The changes of I-V curve IK1 under low K+ or low K+ and Cs+ treatment were similar to the changes of background ones. There were no significant changes in the IK under low K+ superfusion while a remarkable inhibition occurred under low K+ and Cs+ treatment. It was suggested that both IK1 and IK were involved in the induction of EAD under K(+)-free or Cs+ treatment in guinea pig ventricular myocytes.
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