摘要
目的：冠状动脉痉挛（ＣＡＳ）可发生在正常或已有部分狭窄的冠状动脉粥样斑块处，但其对纤溶系统的影响及机制尚不清楚，本研究旨在对此探讨。方法：采用脑垂体后叶素湿敷于犬左冠状动脉前降支外诱发ＣＡＳ的模型。将１５只健康杂种犬随机分为①对照组；②ＣＡＳ组；③冠状动脉部分狭窄＋ＣＡＳ组，观察上述模拟病理状况前后纤溶系统的改变。实验资料用配对ｔ检验。结果：对照组各实验值与其对照值比较无统计学意义（Ｐ＞０．０５）；②组（２次）及③组诱发ＣＡＳ后，与其相应的对照值比较，两组血浆组织型纤溶酶原激活剂（ｔＰＡ）活性及③组的６－酮－前列腺素Ｆ１α水平均显著降低（Ｐ＜０．０１与Ｐ＜０．０５），两组血浆ｔＰＡ抑制物（ＰＡＩ）活性、凝血烷Ｂ２（血栓素Ｂ２，ＴＸＢ２）、肾素活性及③组血浆纤维蛋白原与血管紧张素Ⅱ水平均显著增加（Ｐ＜０．０５或Ｐ＜０．０１）；③组心电图的改变酷似变异性心绞痛和急性心肌梗死。结论：犬实验性ＣＡＳ可导致纤溶系统活性降低，其机制可能主要与血小板活化或内皮细胞损伤有关。
Objective:Coronary artery spasm (CAS) can be induced in normal and in partially stenosed coronary artery,but the effects of CAS on fibrinolytic system and its mechanisms are not clear. This study was aimed to investigate the above problems by animal experiment. Methods:15 healthy hybrid dogs were in randomly divided into control and two CAS groups,i.e. group A,B and C(n=5 in each).CAS was induced by external application of pituitrin(3 IU/application)on the normal(group B) and partially occluded( group C)left anterior descending coronary ariery. Changes of fibrinolytic system were observed before and after the above imitated pathologic states. Experimental data were statistically analysed by means of paired t test. Results;The studied parameters showed no significant difference between the experimental and control values in the control group(p>0.05).After CAS induced by pituitrin applied twice in group B and once in group C,comparing with their corresponding control values plasma levels of tissue type plasminogen activator(tPA)activity in group B and C and 6-keto-PGF1αin group C were significantly decreased(p<0.01 and p< 0.05),and plasma levels of plasminogen activator inhibitor(PAI) activity,thromboxane B2 and renin activity in group B and C and fibrinogen and angiotensin Ⅱin group C showed significant increases(p<0.05 or p<0.01).Changes of electrocardiogram in group C were similar to those of variant angina or acute myocardial infarction. Conclusions:Experimental CAS in dogs can resultin decreased fibrinolytic activity,and its mechanisms may be mainly related to platelet activation or vascular endothelial cell damage.
出处
《中国循环杂志》
CSCD
1996年第2期100-102,共3页
Chinese Circulation Journal
