SYNERGISM BETWEEN FENTANYL PERPHENAZINE METOCLOPORAMIDE AND ACUPUNCTURE

Xu Shaofen, Dong Weiqiang, Zhou Guangzhao, He Xiaoping, Ou Shupei, Sheng Meiping, Wang Miaozhen, Cao Xiaoding

(Research Department of Acupuncture, Shanghai First Medical College, Shanghai)

Wu Jue

(Zhong Shan Hospital, Shanghai First Medical College, Shanghai)

In order to potentiate the effect of acupuncture analgesia (AA), three kinds of drug (fentanyl, perphenazine and metocloporamide) were combined with electro-acupuncture. The potassium iontophoretic colorimetry was used to determine the pain threshold of 203 rabbits. Unilateral "Hegu" and "Waiguan" points of each rabbit were electrically needled with frequency of 1 to 3 pulses/sec. The strength of acupuncture was standardized to elicit muscle twitches, in conscious tranquilizing state. Each drug was administrated intravenously with three grade of dosage - large, medium and small, to observe the effect on AA.

1. The effect of AA was increased and prolonged by  fentanyl. The maximum pain threshold of each dosage plus acupuncture was elevated and there was significant difference from that in acupuncture control group. After stopping of acupuncture, the effect still last 20,40 and over 80 minutes respectively, the acupuncture control group was 40 minutes.

2. The effect of AA was also increased and prolonged by perphenazine. The maximum pain thershold of 0.5mg/kg, I mg/kg or 2mg/kg of perphenazine plus acupuncture group was elevated it was also different from that in acupuncture control group. After stopping acupuncture, the lasting time of each group was over 70,70 and 140 minutes, the acupuncture control group was 50 minutes.

3. The 2mg/kg, 4mg/kg or 6mg/kg of metocloporamide didn't prolong the effect of AA, but only 6mg/kg increased. The maximum pain threshold of 6mg/kg plus acupuncture was elevated (p<0.01). The lasting time of each group was 10,30 and 40 minutes respectively, while the acupuncture control group was none.

This investigation gives the evidence that the drug choice for AA should be based upon the pain mechanism i.e. either acting upon the central opiate receptor or interfering the activity of the central neurotransmitters, such as blocking the brain dopamine receptor or inhibiting the choline esterase.