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安徽医学院生理教研组
Published:1983
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Ma Ruchun, Huang Zhenxin, Shao Qinglan, et al. THE REFLEX REACTION OF CARDIAC HEMODYNAMICS DURING THE PRESSOR REACTION INDUCED BY ACUPUNCTURE[J]. Acupuncture research, 1983, (2): 120-124.
我们曾在猫上观察到针刺“人中”、“足三里”等穴并引起加压反应时
伴有后胺
小肠、肾及脾等区域血管阻力的明显增高
骨骼肌和皮肤容量血管明显收缩
并伴有瞬膜
瞳孔
膀胱及小肠等植物性效应器官的反射反应。本实验旨在观察
针刺引起加压反应时
心脏血流动力学是否也发生变化。为了阐明针刺加压反应的本质
本实验仍与阻断颈总动脉血流及刺激隐神经引起的加压反应的效应相比较。
The work was carried out further to observe if the pressor reaction induced by acupuncture would accompany the reflex reaction of cardiac he- modynamics. Experiment were done on 16 conscious rabbits. The mean bl- ood pressure and the blood flow of aortic arch and central venous pressure were recorded
and then a series of indices of cardiac hemodynamics
for example
stroke volume
heart rate
cardiac index
the stroke volume work done by left ventricle and total peripheral resistance were calculated. During stimulating "Renzhong" and "Zusanli" by repeated intermittent square wave current respectively
the presser reaction appeared
central venous pressure
stroke volume
heart rate and cardiac index did not obv- iously change
but the stroke work done by left ventricle obviously incre- ased ("Renzhong" p<0.05
"zusanli" p<0.001) and total peripheral resis- tance obviously increased
too ("Renzhong" P<0.001
"zusanli" P<0.001). After both vagus nerves were cut
but cardiac sympathetic nerves rema- ined
there was no effect on the change of cardiac hemodynamics accompa- nied by presser reaction of acupuncture. After both stellate ganglia were excised
but vagus nerves remained
acupuncture could still induce obvious presser reaction by the increase of total peripheral resistance
but could no longer induce the increase of the stroke work done by left ventricle. The change of cardiac hemodynamics induced by the stimulation of saphenous. The experimental results show that the pressor reaction of acupuncture is simply induced by the contraction of peripheral blood vessels and then the increase of total peripheral resistance. However
it can accompany the increase of contractility of cardiac muscle by exciting cardiac sympthetic nerves so as to overcome the increase of afterload and maintain the original level of cardiac output.
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