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为研究血小板（ Ｐ Ｌ Ｔ） 中蛋白激酶（ Ｃ Ｐ Ｋ Ｃ） 与缺血性心脑血管病发病的关系。以急性心肌梗塞（ Ａ Ｍ Ｉ） 和脑梗塞病人为对象，检测分析 Ｐ Ｌ Ｔ 中 Ｐ Ｋ Ｃ 底物４０ｋ Ｄ 蛋白磷酸化程度来反映 Ｐ Ｋ Ｃ 活性，并同时设健康对照组。结果疾病组４０ｋ Ｄ 蛋白磷酸化程度明显高于健康对照组，且随凝血酶刺激时间的延长而增强。结果提示 Ｐ Ｋ Ｃ 活性增高为缺血性心脑血管病形成过程中的重要机制之一。
To study the relationship between protein kinase (CPK) in platelets (PLT) and the pathogenesis of ischemic cardiovascular disease. Acute myocardial infarction (AMI) and cerebral infarction patients as the object, detection and analysis of P L T P K C substrate 40k D protein phosphorylation to reflect the activity of P K C, and at the same time set the healthy control group. Results The phosphorylation level of 40kD protein in disease group was significantly higher than that in healthy control group, and increased with the prolongation of thrombin stimulation time. The results suggest that increased P K C activity is one of the important mechanisms in the process of ischemic cardiovascular and cerebrovascular diseases.