Abstract
Alteration in the blood-nerve barrier may be of primary importance in the development of experimental lead neuropathy. Using quantitative track autoradiography, we have directly demonstrated that there is a 15-fold increase in the rate of 210Pb accumulation in the endoneurium 70 days after the onset of chronic intoxication. This change in rate coincides with the appearance of edema but occurs later than the previously demonstrated total endoneurial lead accumulation and later than the onset of segmental demyelination suggesting that, in addition to rate of entry, binding within and exit from this compartment are important determinant of endoneurial lead concentration.
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