V G Kiktev, M Iu Men'shikov, E M Bugriĭ, A V Kuz'min, Iu A Karpov
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引用次数: 0
摘要
采用荧光探针Quin-2 AM研究急性心肌梗死、不稳定型和稳定型心绞痛患者及健康供者血小板钙离子浓度的变化。研究了聚集诱导剂对这些细胞钙离子水平升高过程的影响。急性心肌梗死患者细胞内Ca++浓度在PAF 2.10(-7) M (1337 +/- 255 nM)和ADP 10(-5) M (1767 +/- 296 nM)存在下升高。在不稳定或稳定型心绞痛患者中,钙对刺激剂的反应也有一定的增加。急性心肌梗死患者从第14天开始动态随访,细胞内Ca++浓度明显下降(从1767 +/- 296 nM降至834 +/- 186 nM, p < 0.01)。在治疗过程中,稳定型心绞痛患者血小板对诱导剂的敏感性没有显著变化,而不稳定型心绞痛患者血小板对诱导剂的敏感性有降低的趋势(从707 +/- 274 nM降至410 +/- 95 nM, p > 0.05)。IHD患者血小板聚集性和钙对刺激剂反应的增加是钙代谢紊乱的证据,在疾病的发病机制中起重要作用。
[Calcium metabolism of the thrombocytes in ischemic heart disease].
Changes in Ca++ concentration were studied in platelets of patients with acute myocardial infarction, unstable or stable angina pectoris and those of healthy donors by means of fluorescent probe Quin-2 AM. Influence of aggregation inductors on the process of Ca++ level increase in these cells was also investigated. Intracellular Ca++ concentration increased in patients with acute myocardial infarction in the presence of PAF 2.10(-7) M (1337 +/- 255 nM) and in the presence of ADP 10(-5) M (1767 +/- 296 nM). A certain increase in calcium responses to stimulators was observed also in patients with unstable or stable angina pectoris. Dynamic follow up of patients with acute myocardial infarction starting from the 14th day demonstrated significant fall in intracellular Ca++ concentration (from 1767 +/- 296 nM to 834 +/- 186 nM, p less than 0.01). Platelet sensitivity to inductors during the course of therapy did not change significantly in patients with stable angina pectoris and tended to decrease in those with unstable angina pectoris (from 707 +/- 274 nM to 410 +/- 95 nM, p greater than 0.05). Increase in platelet aggregability and in calcium responses to stimulators in patients with IHD is an evidence of calcium metabolism disturbances which play an important role in the pathogenesis of the disease.