Naloxone reverses inhibitory effect of electroacupuncture on sympathetic cardiovascular reflex responses
Naloxone reverses inhibitory effect of electroacupuncture on sympathetic cardiovascular reflex responses
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DOI：
10.1152/ajpheart.1999.276.6.h2127
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发表时间：
1999-06-01
影响因子：
4.8
通讯作者：
Longhurst, JC
中科院分区：
文献类型：
--
作者：
Chao, DM;Shen, LL;Longhurst, JC
针灸和电针在中医中已被用于治疗包括心绞痛和心肌梗死在内的各种疾病和状况。在反射诱导可逆性心肌缺血的猫模型中，电刺激正中神经模拟电针(内关穴位)可显著改善缺血功能障碍，其次是电针抑制缓激肽(BK)引起的反射加压效应。电针在该模型中的抑制作用的中心机制尚不清楚。相应地，在α-氯醛糖麻醉的猫身上，BK(10mU g/ml)可引起心血管反射反应，显著增加动脉血压和心率(P<；0.05)；超声单晶测微仪测量的正常左心室收缩期壁厚度(%wth)增加31+/-11%(P<；0.05)。结扎冠状动脉左前降支侧支后，对BK的反射加压反应导致缺血区%Th显著降低(-32+/-6%)。电针双侧内关穴时，BK的升压反应受到抑制，局部心肌功能明显改善(+19+/-20%)。静脉注射纳洛酮(0.4 mg/kg；n=9)或延髓头端腹外侧区微量注射纳洛酮(10 nM，0.1亩L，n=14)可逆转电针对血压和%wth的抑制作用。因此，在刺激胆囊期，静脉注射纳洛酮的百分率降至-13+/-29%(P<；0.05)。我们的结果表明，电针对BK诱导的升压反应的抑制作用和随后对缺血功能障碍的改善依赖于阿片受体的激活，特别是位于RVLM的受体。
Acupuncture and electroacupuncture (EA) have been used in traditional Chinese medicine to treat a wide range of diseases and conditions, including angina pectoris and myocardial infarction. In a feline model of reflex-induced reversible myocardial ischemia, electrical stimulation of the median nerves to mimic EA (Neiguan acupoint) significantly improved ischemic dysfunction, secondary to an inhibitory effect of EA on reflex presser effects evoked by bradykinin (BK). The central mechanism of EA's inhibitory effect in this model is unknown. Accordingly in alpha-chloralose-anesthetized cats, BK(10 mu g/ml) was applied to the gallbladder to elicit a cardiovascular reflex response that significantly (P < 0.05) increased arterial blood pressure and heart rate; normalized systolic wall thickening (%WTh) of the left ventricle, measured by ultrasonic single-crystal sonomicrometer, increased by 31 +/- 11% (P < 0.05). After ligation of a side branch of the left anterior descending coronary artery, the reflex presser response to BK resulted in a significant decrease of %WTh (-32 +/- 6%) in the ischemic region. When bilateral EA of the Neiguan acupoints was performed, the presser response to BK was inhibited and regional myocardial function was significantly improved (+19 +/- 20%). The inhibitory effects of EA on blood pressure and %WTh were reversed by intravenous injection of naloxone (0.4 mg/kg; n = 9) or microinjection of naloxone (10 nM in 0.1 mu l/site; n = 14) into the rostral ventrolateral medulla (rVLM). Thus %WTh with intravenous naloxone was reduced to -13 +/- 29% (P < 0.05) during stimulation of the gallbladder. Our results indicate that the inhibitory effect of EA on the BK-induced presser response and the consequent improvement of ischemic dysfunction is dependent on the activation of opioid receptors, specifically receptors located in the rVLM.