THE peripheral neuromuscular pathology of lead has been extensively described in the clinical literature, but the mechanism of lead toxicity which results in neuromuscular impairment is not known1. Early work attempted to locate the site of a toxic lesion in the muscle and showed changes in muscle inorganic phosphate and creatine phosphate levels after lead treatment2,3. Experiments on the superior cervical ganglion, however, suggested that lead affected synaptic transmission by lowering the amount of acetylcholine released on preganglionic stimulation4. In order to separate the effects of lead on nerve from effects on muscle we have carried out experiments using the isolated phrenic nerve-diaphragm preparation.
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