Chronic lead exposure attenuates ethanol-induced hypoalgesia.

Adult male rats were exposed to drinking fluid containing either 500 ppm lead acetate (group lead), or an equivalent concentration of sodium acetate (group control) for 61 days prior to pain reactivity testing using a tail-flick procedure. Rats were placed in restraining tubes for a 20 min acclimation period, and then baseline tail-flick latencies in response to a radiant heat source were measured. Subsequently, half the animals from each group were serially injected IP with either 1.0, 2.0, or 3.0 g/kg body weight of a 20% v/v ethanol solution, and the other half were injected with an equivalent volume of saline. Tail-flick latencies were reassessed at 20-min intervals over the next 2 h. Results indicated dose-dependent ethanol-induced hypoalgesia at all doses, but at the two higher doses the magnitude of the hypoalgesic response was significantly greater in the group control animals than in the group lead animals across the 2-h postinjection period. Results are discussed in terms of an attenuation of the pharmacological properties of ethanol by lead.