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离体孵育的兔耳动脉条受电场刺激后(强度80v,波宽0.5ms,频率8Hz,20min),其亮氨酸脑啡肽(L-ENK)的含量(pg/mg组织湿重)从正常对照值的38.99±17.29降至12.55±1.96(n=12),甲硫氨酸脑啡肽(M-ENK)的含量从正常对照值的134.67±8.11降至73.68±17.96(n=6),下降均十分显著(P<0.001)。用育亨宾阻断α_2受体后,此效应不受影响。动脉条用阿片受体阻断剂纳洛酮或链霉蛋白酶处理后,电场刺激引起的动脉条收缩反应显著增大,但胰蛋白酶无影响。结果表明,耳动脉内源性ENK可因受电场刺激而释放,α_2受体不参与此释放过程;在2～8Hz的实验范围内,随刺激频率的增加ENK释放可能增加。
The rabbit aorta strips incubated in vitro were stimulated by electric field (intensity 80v, wave width 0.5ms, frequency 8Hz, 20min), the content of leucine enkephalin (L-ENK) The content of methionine enkephalin (M-ENK) dropped from 134.67 ± 8.11 of the normal control value to 73.68 ± 17.96 (n = 6) from 38.99 ± 17.29 in the normal control value to 12.55 ± 1.96 (n = 12) , Decreased significantly (P <0.001). With yohimbine blocking alpha 2 receptor, this effect is not affected. Arterioles with opioid receptor blocker naloxone or pronase treatment, the electrical stimulation induced contraction of the artery significantly increased, but no effect of trypsin. The results showed that endogenous ENK in the ear artery could be released by the stimulation of the electric field and α 2 receptor did not participate in the release. ENK release might increase with the stimulation frequency in the range of 2 ~ 8Hz.