We electrophysiologically examined the effect of the PGI2 analogue, Beraprost sodium (BPS), on neuropathy in spontaneously diabetic WBN/Kob rats, Diabetic male WIIN/Kob rats, aged 43 to 45 weeks, were randomly divided into BPS-treated (n=7) and untreated (n=6) groups. BPS was orally administered at a dose of 30μg/kg every day, while untreated rats were given distilled water, for 16 weeks. Motor nerve conduction velocity (MNCV) of the tail nerve and the coefficient of variation (CV) of pulse intervals of the tail artery, as indicators of parasympathetic nerve function, were determined before and after treatment. After the 16 week treatment period, the sciatic nerve blood flow (NBF) was measured by laser doppler flowmetry. At the end of treatment, the CV of pulse intervals of the tail artery in the BPS treated group was significantly increased in comparison with that in the untreated group, while there was no significant difference in MNCV between the two groups. In addition, NBF in the BPS-treated group was increased in comparison with that in the untreated group. In conclusion, these results suggest that BPS treatment might be useful not only for peripheral neuropathy but also for autonomic neuropathy.
The effects of elevated glucose and eicosapentaenoic acid ethyl ester on in vitro 2 [3H] myoinositol uptake were evaluated in cultured rat vascular smooth muscle cells (VSMC).Since Na+-deprivation and the addition of ouabain (1mM) are known to reduce myo inositol uptake, we speculated that myo-inositol incorporation into VSMC might be dependent on an active transport system mediated by Na+-K+ATPase activity. Glucose inhibited myo inositol uptake in a dose-dependent manner. However, the addition of eicosapentaenoic acid ethyl ester (3×104M) prevented this glucose mediated inhibition of myo inositol uptake. These results suggest that eicosapentaenoic acid supplementation may prevent or ameliorate myo inositol related disorders in diabetics.
Although the measurement of beatto-beat heart rate variation is generally accepted as a valid test, there is still considerable debate as to which currently available method is the most practical for general clinical use. This study was designed to assess which test is most suitable in terms of the relationship with diabetic neuropathy. Three different methods of analysing RR interval (heart rate) variation were compared in 16 normal subjects and 48 diabetics with responses to diabetic neurological measurements such as achilles tendon reflex, blood pressure fall on standing, and motor conduction velocity of the tibial nerve. The subjects selected were all in their 40s so as to exclude the influence of age as much as possible. Hinge spread of RR intervals on deep breathing differentiated most accurately not only between normal subjects and diabetics, but also between diabetics with and without neurological damage. The coefficient of variation of RR intervals at rest and the difference between the maximum and minimum heart rates on deep breathing did not differentiate groups more accurately than the hinge spread of RR intervals. Therefore, for routine clinical usage, we conclude that recording the hinge spread of RR interval variation on deep breathing is the most practical method currently available.