Abstract
Research has shown that animals exposed to cadmium or lead self-administer a set volume of ethanol in an operant context at lower rates than their control counterparts, suggesting a reduction in the reward value of the drug. The present paper seeks to determine whether this pharmacologic attenuation extends to hypoalgesia, a physiologic consequence of acute ethanol exposure. Specifically, in Experiment 1, rats exposed to either 0 or 100 ppm cadmium (as cadmium chloride) were injected with doses of 0.5, 1.0, 1.5 and 2.0 g/kg, and tail-flick latencies were recorded every 20 min over the next 2 hr. Results of Experiment 1 indicated ethanol induced hypoalgesia at both the 1.5 and 2.0 g/kg doses for control animals, but ethanol-induced hypoalgesia was evident only at the highest dose for the cadmium-treated rats. Further, the magnitude of hypoalgesia was significantly diminished among cadmium-treated rats. In Experiment 2, the same procedure was used on rats exposed to either 0 or 500 ppm lead acetate at doses of 1.0, 2.0, and 3.0 g/kg ethanol. Results indicated ethanol-induced hypoalgesia at all doses. However, similar to the cadmium-exposed animals, at the 2.0 and 3.0 g/kg doses lead-treated animals exhibited less ethanol-induced hypoalgesia than control animals. Results are discussed in terms of an attenuation of the pharmacologic properties of ethanol by cadmium or lead.
Burkey, Robert Trent (1993). The effects of cadmium and lead on ethanol-induced hypoalgesia. Master's thesis, Texas A&M University. Available electronically from
https : / /hdl .handle .net /1969 .1 /ETD -TAMU -1993 -THESIS -B959.