Elevation of vascular endothelial growth factor-A serum levels following acute myocardial infarction. Evidence for its origin and functional significance
Elevation of vascular endothelial growth factor-A serum levels following acute myocardial infarction. Evidence for its origin and functional significance
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DOI：
10.1006/jmcc.1999.1062
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发表时间：
2000-01-01
影响因子：
5
通讯作者：
Waltenberger, J
中科院分区：
文献类型：
--
作者：
Kranz, A;Rau, C;Waltenberger, J
急性心肌梗死（AMI）发病后，许多血清参数显示出明确的变化，反映心肌损伤。在连续的修复阶段期间，启动补偿过程，包括基于血管生成和动脉生成的侧支循环的形成。血管内皮生长因子-A（VEGF-A）是一种重要的血管生成因子，在缺血心肌中表达上调，但急性心肌缺血是否导致血清VEGF-A浓度升高尚不清楚。此外，在一小组亚急性心肌梗死患者中，测定冠状窦血液中VEGF-A的浓度。在AMI组中，在AMI发作后第1天测得血清VEGF-A为105 [78：176] pg/ml，第3天测得血清VEGF-A为114 pg/ml [72：163] pg/ ml。AMI后第7天血清VEGF-A水平显著升高至189 [119; 373] pg/ml（P = 0.0103），第10天升高至255 [162：371] pg/ml（P = 0.0007）。健康对照组和不稳定型心绞痛患者血清VEGF-A水平分别为98 [75; 137] pg/ml和116 [57; 140] pg/ml。AMI后第10天的血清分别含有能够刺激内皮细胞增殖的生物学相关浓度的VEGF-A。令人惊讶的是，VEGF-A血清水平在取自冠状窦的样品中相似，为61 [43; 83] pg/ml。因此，血流中VEGF-A的主要来源不是梗死心肌。然而，血小板（VEGF-A的丰富来源）的数量在心肌梗死后显著增加，即284 [252：363] x 10（9）/升vs 220 [177：363] x 10（9）/升。250] x 10（9）/升。AMI后VEGF-A升高的时间进程强烈提示VEGF-A在人心脏中起着冠状动脉侧支形成的内源性激活剂的作用。VEGF-A升高最可能的来源是血小板，而不是梗死心肌。(C)北京大学出版社.
Following the onset of acute myocardial infarction (AMI), a number of serum parameters show well-defined changes reflecting myocardial injury. During the consecutive repair phase, compensatory processes are initiated including the formation of a collateral circulation on the basis of angiogenesis and arteriogenesis. An important angiogenic factor is vascular endothelial growth factor-A (VEGF-A), shown to be upregulated in the ischemic myocardium, It is unclear, however, whether acute myocardial ischemia leads to a detectable elevation of VEGF-A serum concentrations.With the use of an immunoradiometric assay, we measured the levels of VEGF-A in the serum of patients after AMI at defined lime intervals, of patients with unstable angina pectoris (UAP) and of healthy individuals, In addition, in a small group of patients with subacute myocardial infarction VEGF-A concentrations were measured in coronary sinus blood. The data are given as median followed by the 25th and 7th percentiles.In the group with AMI serum VEGF-A measured 105 [78: 176] pg/ml on day 1 and 114 pg/ml [72; 163] pg/ ml on day 3 after onset of AMI. Serum levels of VEGF-A significantly increased on day 7 after AMI to 189 [119; 373] pg/ml (P = 0.0103) and on day 10 to 255 [162: 371] pg/ml (P = 0.0007). The VEGF-A serum level in healthy controls and in patients with UAP measured 98 [75: 137] pg/ml and 116 [57; 140] pg/ml. respectively, Serum at day 10 after AMI contained VEGF-A at a biologically relevant concentration capable of stimulating proliferation of endothelial cells. Surprisingly, VEGF-A serum levels were similar in samples taken from the coronary sinus with 61 [43; 83] pg/ml. Therefore the main source for VEGF-A in the blood stream is not the infarcted myocardium. However, the number of platelets, a rich source of VEGF-A, is significantly increased after myocardial infarction, i.e. 284 [252: 363] x 10(9)/litre v 220 [177: 250] x 10(9)/litre.In conclusion, the time course of VEGF-A elevation following AMI strongly suggests that VEGF-A plays a role as an endogenous activator of coronary collateral formation in the human heart. The most likely source of the elevated VEGF-A are platelets, rather than the infarcted myocardium. (C) 2000 Academic Press.