The dependence of the conduction velocity of the action potential on the spike interval from a preceding potential was studied using human single motor units during voluntary muscle contraction. The spike potential was recorded from the surface of the skin overlying M. vastus medialis by use of surface electrodes (diameter 5 mm). The results were as follows: Conduction velocity increased with a decrease in spike interval. The relation between conduction velocity and spike interval can be expressed as log v = kt + a, where v is conduction velocity (m X s-1), t is spike interval (ms) and k and a are constants. All data can be expressed by the above formula with a highly significant correlation. After arterial occlusion, there was little or no relation between conduction velocity and spike interval. This lack of correlation between these parameters was not restored to the initial correlation within a period of 15 min. Effects similar to occlusion could be seen in the result of prolonged isometric contraction. However the lack of correlation between these parameters was restored to the initial correlation within a 15 min recovery period. At low muscular temperature, the relation could not be described by a logarithmic regression. As the spike interval became shorter, the conduction velocity decreased. After cessation of cooling, the relation was restored to the initial correlation within 30 min. The mechanisms of these changes are still uncertain but some possible factors can be considered, for example, composition of the extracellular fluid, pH, temperature and permiability of the excitable membranes of the muscle.
The Long-Evans Cinnamon (LEC) rat is a mutant strain of rats that accumulate copper (Cu) in the liver in much the same way as individuals who suffer from Wilson's disease (WD) and has been suggested as a model for this disease. Lipid peroxidation (LPO) is considered to be involved in the toxic action of Cu in the livers of LEC rats. We investigated the mechanism of LPO in the livers of LEC rats showing apparent signs of hepatitis. Several-fold higher LPO levels were observed in post-mitochondrial supernatant (S-9) fraction of livers from hepatitic LEC rats than in those from Wistar rats. To mimic living cells, we introduced NADPH-generating system (NADPH-gs) into the S-9 incubation system. Thus was ensured a constant supply of NADPH to vital enzymes that may be directly or indirectly involved in the generation and/or elimination of reactive oxygen species (ROSs), such as glutathione reductase (GSSG-R), which require NADPH for their reactions. The levels of LPO in liver S-9 from hepatitic LEC rats were further increased by incubating liver S-9 at 37 degrees C in the presence of NADPH-gs. This increase was inhibited by EDTA, butylated hydroxytoluene (BHT), and catalase (CAT), suggesting that some metal, most likely the accumulated Cu, and ROSs derived from hydrogen peroxide (H2O2) are involved in the increased levels of LPO in the livers of hepatitic LEC rats. The requirement of NADPH-gs for enhanced LPO in the livers of hepatitic LEC rats indicates the consumption of NADPH during reactions leading to LPO. It is known that H2O2, and consequently hydroxyl radical are generated during Cu-catalyzed glutathione (GSH) oxidation. The cyclic regeneration of GSH from GSSG by NADPH-dependent GSSG-R in the presence of NADPH-gs may cause sustained generation of hydroxyl radical in the presence of excess free Cu. The generation of H2O2 in S-9 fraction of livers from hepatitic LEC rats was observed to be significantly higher than that in S-9 fraction of livers from non-hepatitic LEC rats and Wistar rats. Moreover, in addition to the reported decrease in glutathione peroxidase (GPX) activity, we found that CAT activity was markedly decreased in LEC rats with hepatitis. The increased generation of H2O2 with reduced activities of GPX and CAT may result in cellular accumulation of H2O2 in the liver of hepatitic LEC rats. Taken altogether, it is suggested that the accumulated H2O2 undergoes the Fenton-type reaction with also accumulated free Cu, thus generating hydroxyl radical in the livers of hepatitic LEC rats and increasing LPO levels in these animals.
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