[Intrathoracic implantation of permanent pacemaker in a 81-day-old infant for congenital complete heart block (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Nagano.
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The effects of changing the intracellular pH on the action potential duration and other electrophysiological properties were studied in squid giant axons perfused intracellularly with TEA(tetraethylammonium)-containing solutions and under Ca-Na bi-ionic conditions. The duration of the action potential plateau, produced by TEA, was markedly decreased with acidic intracellular solutions and increased with alkaline intracellular solutions. The normalized duration, d, was calculated by dividing the plateau duration by that of the standard intracellular pH of 7.3, and plotted against the intracellular pH. The curve could be expressed by the formula log [d/(D-d)] = n(pH-pK') where D is the saturated value of d, n a constant and pK' the value of pH at which d becomes D/2. The values selected for D and n were 2.6 and 1.4, respectively. The pK' was found to be 7.5. Lowering of the extracellular pH to 6.2 only slightly changed the plateau duration. Voltage clamp analysis revealed that acidic intracellular solutions decreased the size of the inward current and the slope conductance which were measured at the late period of the depolarizing clamping pulse. Alkaline intracellular solutions increased the size of the inward current and the slope conductance measured at this late period. Intracellular perfusion with a low pH solution also shortened the duration of the Ca-Na bi-ionic action potential. It is argued that the remarkable generality of the pH effect on the plateau duration implies the existence of a common mechanism of formation of the plateau under widely differing experimental conditions.
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The alteration of glycoprotein in the glomerular basement membrane in diabetic glomerulosclerosis was studied with preparative polyacrylamide gel electrophoresis by Uniphor column. Normal glomerular basement membrane was fractionated into 32 glycoprotein fractions. Decrease in sialic acid residue of sialoprotein was the characteristic finding observed in diabetic glomerulosclerosis. A hypothesis which explains the alteration of sialoglycoprotein is proposed.
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The mechanism of post-tetanic hyperpolarization (PTH) occurrence was investigated using the intracellar recording technique. The median giant axon of a crayfish abdominal nerve cord was repetitively stimulated to elicit PTH. When the membrane potential was hyperpolarized by intracellularly applied currents, PTH reversed its sign. K+ removal from the external medium increased the size of PTH and shifted its reversal potential in the hyperpolarizing direction. This results shows that an increase in K+ conductance contributes to the formation of PTH. In a K+-free medium, the size of PTH was reduced by replacement of Na+ with Li+ in the external medium, by application of ouabain or DNP, or by cooling. These procedures shifted the reversal potential in the depolarizing direction. These findings are interpreted as showing that, with K+ absent, PTH is partly due to the activity of electrogenic Na pump. With lowering of external Na+ concentration, PTH became larger and the reversal potential moved in the hyperpolarizing direction. The experiment suggests that Na+ conductance is also increased when PTH is elicited because one expects the amount of Na+ entering per impulse and the activation of the Na pump to be reduced by reducing Na+ concentration in the external medium. It is concluded that PTH in the median giant axons of crayfish is produced by at least two mechanisms. One is an increase in activity of the electrogenic Na pump, and the other is an increase of membrane conductance to K+ and Na+.
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