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中国中医研究院针灸研究所
纸质出版日期:1993
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文琛, 曹庆淑, 瞿娜, 等. 电针对急性心肌缺血的微血管酶和儿茶酚胺荧光的作用[J]. 针刺研究, 1993,(3):223-227.
Wen Shen Cao Qingshu Zhai Na Jiang Jin Ma Huiming Chen Shuping Han Zhenjing. Effect of EA on the Enzymes of Microvasculature and CA Fluorescence in Acute Myocardial Ischemia[J]. Acupuncture research, 1993, (3): 223-227.
以碱性磷酸酶(ALP)、镁激活的腺苷三磷酸酶(Mg
(2+)
-ALP_(ase))和儿茶酚胺(CA)荧光组化方法观察了电针对急性心肌缺血作用的机理。结扎左冠状动脉心室支30分钟后
缺血心肌中以 ATP 显示的毛细血管大为减少
长度缩短;而缺血电针组则有显著意义增加
说明电针对缺血心肌微循环和转运功能的改善。Mg(2+)-ALP_(ase))和儿茶酚胺(CA)荧光组化方法观察了电针对急性心肌缺血作用的机理。结扎左冠状动脉心室支30分钟后
缺血心肌中以 ATP 显示的毛细血管大为减少
长度缩短;而缺血电针组则有显著意义增加
说明电针对缺血心肌微循环和转运功能的改善。Mg
(2+)
-ATP_(ase)可显示心肌微血管的质膜和基膜;经显微分光光度计测量
Mg(2+)-ATP_(ase)可显示心肌微血管的质膜和基膜;经显微分光光度计测量
Mg
(2+)
-ATP_(ase)在缺血电针组比缺血对照组光密度增加
这可加强缺血心肌 Na(2+)-ATP_(ase)在缺血电针组比缺血对照组光密度增加
这可加强缺血心肌 Na
+
K+K
+
离子跨膜转动功能。心肌儿茶酚胺荧光所显示的交感肾上腺素能膨体神经末梢;缺血后减少或耗竭
电针组则较多而亮
这有益于加强缺血心肌的收缩力。It was aimed at observing the histochemical basis of physiological experiment about the effectof electroacupuncture(EA)on acute myocardial ischemia(AMI)in this paper.The capillaries ofmyocardium were reflected with both alkaline phosphatase(ALP)and Mg+离子跨膜转动功能。心肌儿茶酚胺荧光所显示的交感肾上腺素能膨体神经末梢;缺血后减少或耗竭
电针组则较多而亮
这有益于加强缺血心肌的收缩力。
It was aimed at observing the histochemical basis of physiological experiment about the effectof electroacupuncture(EA)on acute myocardial ischemia(AMI)in this paper.The capillaries ofmyocardium were reflected with both alkaline phosphatase(ALP)and Mg
(2+)
-ATP_(asc).Thirty minafter ligating the left ventricular branch(LVB)
the capillaries stained by ALP were much de-creased in the ischemic group without EA
while in EA group they were increased distinctly.Thenumber and the total length of the capillaries in a 220×320μm ischemic area of the posterior wall(section 10μm)were measured and compared.In ischemic group the number was 17.2±1.65
the length was 634.62±666.24μm
in EA group 22.5+1.44
1187.57+103.69μm
respectively.Both counts were significant differences(P
<
0.05
P
<
0.001).It reflected that EA could improvethe microcirculation and metabolic function of AMI.Mg(2+)-ATP_(asc).Thirty minafter ligating the left ventricular branch(LVB)
the capillaries stained by ALP were much de-creased in the ischemic group without EA
while in EA group they were increased distinctly.Thenumber and the total length of the capillaries in a 220×320μm ischemic area of the posterior wall(section 10μm)were measured and compared.In ischemic group the number was 17.2±1.65
the length was 634.62±666.24μm
in EA group 22.5+1.44
1187.57+103.69μm
respectively.Both counts were significant differences(P
<
0.05
P
<
0.001).It reflected that EA could improvethe microcirculation and metabolic function of AMI.Mg
(2+)
-ATPase was shown on the plasmmembrance of endothelial cell of microvasculature and analysed quantitatively with a Univar scanning microspectrophotometer.After occluding LVB for 30 min its optic density of AMI was de-creased to 106.834-14.06
while it was increased to 210.83+24.88 in EA group
P
<
0.05.Theactivity of Mg(2+)-ATPase was shown on the plasmmembrance of endothelial cell of microvasculature and analysed quantitatively with a Univar scanning microspectrophotometer.After occluding LVB for 30 min its optic density of AMI was de-creased to 106.834-14.06
while it was increased to 210.83+24.88 in EA group
P
<
0.05.Theactivity of Mg
(2+)
-ATPase could increase in transporting Na(?)
k(?)ions through the membrance ofthe endothelial cells of ischemic myocardium.The result was consistent with the physiolgical ex-periment
because EA could regulate the changes of mean repolarization rate induced by AMI andadjust the ion concentration of transmembrane.The catecholamine(CA)in myocardium was lo-cated at sympathetic adrenergic terminals with varicosities containing norepinephrine(NE).Thirty rain after ligating LVB
the fluorescence of adrenergic terminals was decreased and/or de-pleted
but in EA group
the fluorescent varicosities were increased gradually.It was benficial tostrengthing the contractibility of myocardium.
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