摘要
为探求急性心肌梗塞冠状动脉再通后,抗凝护心Ⅰ号缓解再
灌注后血液高凝状态及血管痉挛的机理和疗效,建立了大鼠急性
心梗再灌注模型,分别给予生理盐水,抗凝护心Ⅰ号正常剂量,
高剂量,阿斯匹林,抗凝护心Ⅰ号正常剂量与阿斯匹林合剂,检
测大鼠凝血指标及血管活性物质变化。
结果显示,抗凝护心Ⅰ号高剂量组与抗凝护心Ⅰ号正常剂量
合阿斯匹林组能明显提高血浆纤溶酶原激活物(tPA)的活性水
平,显著降低纤溶酶原激活剂抑制物(PAI)活性水平,显著降
低血栓素B_2(TXB_2)的含量。Ⅰ号正常剂量、Ⅰ号高剂量、Ⅰ号
正常剂量与阿斯匹林合剂均能显著增加一氧化氮(NO)含量,并
能显著降低血浆内皮素(ET)含量。因此说明,抗凝护心Ⅰ号是
具有良好抗凝血功效的中药制剂,防止AMI溶栓后血液的高凝状
态,激活纤溶系统,避免再梗塞的发生;抗凝护心Ⅰ号可使引起
血管痉挛收缩的血管活性物质ET减少,使内皮依赖性血管舒张
因子(EDRF)NO的含量升高,故可缓解血管痉挛,舒张血管,恢
复心肌供血,防止溶栓后血管痉挛及血液高凝状态引起的再梗塞
可能。
ABSTRACT
In order to study the mechanism and curative effect of
Kang Ning Hu Xin?(KNHX條)on alleviating the blood
hypercoagulation state and release the spasticity of blood
vessel, We established on rats the model of acute myocardial
infarction and ischemia梤eperfusion. Forty rats were
randomly divided into five groups. They were respectively
given the normal saline, normal dosage of KNHX條, high?
dosage of KNHX條, aspirin, mixture of KNHX條 and aspirin.
Through the experiment, We examine the variability of the
coagulating index and of some active blood vessel matters.
The results were as follows high-dosage of KNHX條,
mixture of KNHX條 and aspirin (MKA) could markedly increase
the plasma levels of tissue type plasminogen activator (tpA)
and decrease the plasma levels of plasminogen activator
inhibitor (PAI).They three could also decrease the plasma
contents of thromboxane B2 (TXB2).Normal梔osage of KNHX-
1,high梔osage of KNHX條,mixture of KNHX1 and aspirin (MKA)
could increase the contents of nitric oxide (NO)and they
could also obviously decrease the plasma contents of
endothelin(ET).
We Can draw a conclusion that traditional chinese
medicine KNHX條 is a good anti梒oagulant; KNHX? could
prevent the hypercoagulation state after acute myocardial
infarct ion and avoid the occurance of re梚nfarction; KNHX1
could decrease the contents of endothelin Which could lead
to spasm of blood vessel and increase the contents of nitric
oxide which can release the spasm of blood vessel and
improve the blood supply of cardiac musle. So, KNHX條 can
prevent the spasm of the blood梫essel and avoid the re?
4
infarction after the dissolving of thrombus because of
blood hypercoagulation state.
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