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1. 复旦大学医学院针刺原理研究所
2. 复旦大学医学院针刺原理研究所 医学神经生物学国家重点实验室,上海,200032
3. 医学神经生物学国家重点实验室,上海,200032
纸质出版日期:2002
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高焕民, 程介士. 侧脑室注射孤啡肽对电针抗脑缺血作用的影响[J]. 针刺研究, 2002,(1):20-24.
Influence of Orphanin FQ Intracerebroventricular Administration on Electroacupuncture's Anti-cerebral Ischemic Effect in Rats[J]. Acupuncture research, 2002, (1): 20-24.
目的 :本工作试图阐明孤啡肽 (OFQ)在脑缺血中的作用
并观察它对针刺抗脑缺血的影响。方法 :采用大鼠大脑中动脉栓塞模型
应用侧脑室注射方法以体感诱发电位 (SEP)和脑梗塞体积为指标观察了不同剂量的孤啡肽对脑缺血的作用
以及对针刺抗脑缺血的影响。结果 :大鼠大脑中动脉栓塞后SEP波幅降低
侧脑室注射 1 0 μg和 1 μg孤啡肽均进一步降低SEP的波幅
对照组在再灌后 1hrSEP基本恢复
而侧脑室注射孤啡肽 1 0 μg直到再灌后 3hr仍不恢复。注射剂量与SEP反应呈一定的量 效关系
即剂量越大
SEP抑制越显著。同时增大了脑梗塞灶的体积。而相同条件下侧脑室注射 0 .1 μg孤啡肽SEP的波幅和脑梗塞灶的体积与对照组比较无显著性差异。电针能减小脑梗塞体积
增大SEP的波幅。侧脑室注射 1 μg孤啡肽后针刺效应减弱
表现为SEP的波幅降低
脑梗塞灶的体积增大。结论 :侧脑室注射孤啡肽可加重脑缺血
且减弱了针刺抗脑缺血的作用。
Objective: To verify the effect of Orphanin (O) FQ on cerebral ischemia and observe its influence on electroacupuncture(EA)'s anti cerebral ischemia. Methods: 63 SD rats were randomly divided into sham operation (control) group (n=5)
cerebral ischemia group (n=8)
OFQ 10 μg group (n=7)
OFQ 1 μg group (n=7)
saline group (n=8)
EA+ OFQ 1 μg group (n=8)
EA+saline group (n=7) and EA group (n=6). Cerebral ischemia model was established using the cerebral middle artery occlusion (MCAo) method. "Shuigou"(GV 26) and "Baihui" (GV 20) were stimulated with EA (dense sparse waves
3.85~6.25 Hz
1.4~2 mA) for 60 min. Cerebral somatosensory evoked potential(SEP) was recorded and cerebral infarct volume detected. Thirty minutes after MCAo
OFQ (10 μg/10 μL
1 μg/10 μL
0.1 μg/10 μL) and saline 10 μL were injected into the right lateral cerebroventricle via an implanted catheter. Results: Following cerebral ischemia
the amplitude of SEP decreased
and after intracerebroventricular (icv) administration of OFQ 10 μg and 1 μg respectively
SEP declined further. One hour after cerebral ischemia reperfusion
SEP recovered basically
while that of OFQ 10 μg group remained low level even 3 hr after ischemia reperfusion. A certain dose effect correlation was found between OFQ and SEP suppression reaction. Application of OFQ enlarged the infarct volume
but after icv of OFQ 0.1 μg
changes of the SEP amplitude and infarct volume had no significant difference compared with those of control group (P>0.05). Following icv of OFQ 10 μg and 1 μg
cerebral infarct volume increased considerably in comparison with that of cerebral ischemia group (P<0.05). Following cerebral ischemia
the amplitude of SEP in control group lowered from 71.46±6.42% to 27.64±6.26%
while in EA group
that of SEP decreased from 81.12±4.51% to 55.64±8
81%
existing a significant difference between these two groups (P<0.05); SEP amplitude of EA+OFQ group was significantly lower than that of EA+saline group (P<0.01). The cerebral infarct volumes in ischemia group and EA group were 24.18±1.08 mm 3 and 18.497± 5.112 mm 3 respectively. Following icv OFQ
the cerebral infarction volume EA+OFQ 1 μg group was remarkably larger than that of EA+saline group
suggesting an inhibitory action of OFQ on EA's anti cerebral ischemia. Conclusion: Orphanin FQ 10 μg and 1 μg (icv) deteriorates the degree of ischemic brain damage and reverses the anti cerebral ischemic effect of EA in the adult SD rats.
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