脊髓中血管紧张素Ⅱ的释放及其抗电针镇痛

ANGIOTENSIN Ⅱ RELEASE AND ANTIELECTROACUPUNCTURE ANALGESIA IN SPINAL CORD

本文采用放射免疫分析方法测定不同频率电针引起大鼠脊髓液中血管紧张素Ⅱ（ＡⅡ）免疫活性（ｉｒ）的变化，并观察阿片受体在其中起的作用。结果表明：（１）２Ｈｚ电针时大鼠脊髓灌流液中ＡⅡ－ｉｒ减少２０％，但无立计学意义；１５Ｈｉ电针使灌流液中ＡⅡ－ｉｒ降低６２％（Ｐ＜０．０１）；１００Ｈｉ时ＡⅡ－ｉｒ增加６０％（Ｐ＜０．０５）。（２）脊髓蛛网膜下腔（ｉ．ｔ．）注射阿片受体桔抗剂纳洛酮后，１５Ｈｚ电针反使灌流液中ＡⅡ含量增加１２５％（Ｐ＜０．０５）。（３）特异性μ受体激动剂ｏｈｍｅｆｅｎｔａｎｙｌ可以抑制ＡⅡ释放，δ和Ｋ激动剂无效。（４）ｉ．ｔ．注射ＡⅡ受体拮抗剂ｓａｒａｌａｓｉｎ明显加强１００Ｈｚ电针镇痛（Ｐ＜０．０５），但对２Ｈｚ和１５Ｈｚ电针针效影响不大。结果提示：ＡⅡ拮抗剂与电针合用可能有助于加强１００Ｈｚ电针的镇痛效果。内源性阿片肽通过μ受体抑制电针期间ＡⅡ的释放。

Changes in the content of angiotensin Ⅱ (A Ⅱ ) immunoreactivity (ir) in ratspinal perfusate induced by electroacupuncture (EA) stimulation of different frequencies were measuerd by radioimmunoassay (RIA). The results were analyzed in relationto the role of opioid recepor. (1) 2 Hz EA produced a 20% (P>0. 05) decrease inA Ⅱ-ir content in the spinal perfusate. 15 Hz EA produced an even more decrease(62 %, P< 0. 01 ), whereas 100 Hz produced a significant increase (65%, P <0. 05 ). (2) The release in spinal A Ⅱ-ir produced by 15 Hz EA was reversed by the opioid antagonist naloxone to a of 125% highter than that of the control (P<0. 05), suggesting that 15 Hz EA may accelerate the release of endogenous opioids to suppress therelease of A Ⅱ. (3) This was substantiated by the finding that intrathecal (i. t. ) injection of the selective mu agonist ohmefentanyl produced a dramatic suppression (20%,P<0. 05) of A Ⅱ release, but not by delta and kappa agonist. (4) Intrathecal injectionof salarasin, the angiotensin receptor antagonist, produced a significant potentiation ofthe analgesia produced by 100 Hz EA, but not that produced by 2 or 15 Hi EA. It isconcluded that 15 Hz EA may induce the release of endogenous opioids acting on μ opioid receptor so as to suppress A Ⅱ release, and that 100 Hz EA may acceleate the release of A Ⅱ serving as a brake for 100 Hz BA-induced analgensia. Removal of thebrake by angiotensin antagonist may be advised as an adjunct for the potentiation of100 Hz EA-induced analgesia.