We measured changes in membrane potential (MP), extra-and intracellular potassium and intracellular sodium ion activities (4, 4, and aNa) in papillary muscle of the guinea-pig heart induced by repetitive stimulation at various frequencies and periods in vitro, using doublebarrelled ion-selective microelectrodes. Stimulation (2-4 Hz) depolarized the cells, and termination of stimulation induced hyperpolarization. The a K and aNa (stimulated at 0.2 Hz) were 92.3 + 4.6 and 7.8 ± 2.0 mM (mean + S.D.), respectively. Prolongation of the stimulation period (0.5-2 min) increased aNa time-dependently, but there was no further increase by stimulation for longer than 3 min. The increase in aNa was dependent on stimulus frequency. After termination of the stimulation, aNa declined exponentially. a K slightly decreased by the stimulation (3-4 Hz). a K increased during the stimulation period, and decreased below the initial level after termination of the stimulation. Results suggest that in guineapig papillary muscle, the. contribution of an electrogenic component of Na-K pump to the hyperpolarization after stimulation would be small, since the hyperpolarization could be explained mostly by depletion of 4 induced by Na-K pump activity.
Two cases of hepatocellular carcinoma (HCC) were described, in whom hypercholinesterasemia was found. Histochemical examinations revealed that there was a significantly increase in enzyme activity of cholinesterase in liver tissue slice obtained from the part of carcinoma in case 1. It was found that cholinesterase activity in homogenized liver tissue in part of carcinoma was much higher than that of non-carcinoma, and even in other HCC cases, hepatic cirrhosis and control liver tissues. These results suggested that HCC cells were capable of producing cholinesterase and, therefore, that hypercholinesterasemia was an additional paraneoplastic syndrome in HCC.
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