Tissue factor and its inhibition at the human microvascular anastomosis.
Tissue factor and its inhibition at the human microvascular anastomosis.
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组织因子及其对人体微血管吻合的抑制作用。
DOI：
10.1006/jsre.1996.0041
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Johnson,PC
中科院分区：
文献类型：
--
作者：
Dumanian,GA;Heil,BV;Khouri,RK;Hong,C;Labadie,K;Wun,TC;Johnson,PC
手术形成的血管吻合是一个病因不明的血栓形成区。本研究旨在探讨组织因子作为人体微血管血栓形成原因的重要性。还在该全血管模型系统中测试了组织因子途径抑制剂（TFPI）阻断组织因子作用的能力。在存在和不存在TFPI的情况下，在离体人胎盘动脉的腔表面、外膜表面以及微血管吻合部位测定组织因子活性。在存在和不存在TFPI的情况下测量血管壁凝血酶活性。血小板沉积到血管表面上使用灌注系统进行测量与TFPI。外膜组织因子活性（4.6 ± 2.8 × 10− 4单位Xa产生/min）高于内皮（1.8 ± 1.6 × 10−4，P< 0.03）或手术吻合处（2.1 ± 1.2 × 10−4，P< 0.04）。TFPI使23个内皮、外膜和吻合段中的21个的Xa生成降至不可检测水平（P< 0.002）。与对照组相比，TFPI显著降低血管壁凝血酶活性（对照组，3.2 ± 1.7 ng FPA/（ml × min）; TFPI，1.4 ± 1.2 ng FPA/（ml × min）;P< 0.0001）。TFPI可减少血小板在内皮完整血管段的沉积（无TFPI，0.88 ± 0.69 × 106个血小板/cm 2; TFPI，0.49 ± 0.29 × 106个血小板/cm 2;P= 0.06）和有血管病变的血管段（无TFPI组，1.3 ± 0.70 × 106血小板/cm ~ 2; TFPI组，0.76 ± 0.35 × 106血小板/cm ~ 2;P< 0.02）。本研究证明了组织因子作为人全血管模型系统中血栓形成元素的重要性。TFPI可有效降低这种血栓形成性。
The surgically created vascular anastomosis is a thrombogenic zone of uncertain etiology. This study was designed to investigate the importance of tissue factor as a cause of human microvascular thrombogenicity. The ability of tissue factor pathway inhibitor (TFPI) to block the effect of tissue factor was also tested in this whole-vessel model system. Tissue factor activity in the presence and absence of TFPI was assayed on the luminal surface of dissected human placental arteries, on the advential surface, and also at the site of a microvascular anastomosis. Vessel wall thrombin activity was measured in the presence and absence of TFPI. Platelet deposition onto a vessel surface using a perfusion system was measured with and without TFPI. Tissue factor activity was greater on the adventitia (4.6 ± 2.8 × 10−4units factor Xa generated/min) than on the endothelium (1.8 ± 1.6 × 10−4,P< 0.03) or at a surgically created anastomosis (2.1 ± 1.2 × 10−4,P< 0.04). TFPI reduced Xa generation to undetectable levels in 21 of 23 endothelial, adventitial, and anastomotic segments (P< 0.002). TFPI significantly reduced vessel wall thrombin activity in comparison to control anastomoses (control, 3.2 ± 1.7 ng fibrinopeptide A (FPA)/(ml × min); TFPI, 1.4 ± 1.2 ng FPA/(ml × min);P< 0.0001). TFPI reduced the platelet deposition on vessel segments with intact endothelium (no TFPI, 0.88 ± 0.69 × 106platelets/cm2; TFPI, 0.49 ± 0.29 × 106platelets/cm2;P= 0.06) and on vessel segments with anastomoses (no TFPI, 1.3 ± 0.70 × 106platelets/cm2; TFPI, 0.76 ± 0.35 × 106platelets/cm2;P< 0.02). This study demonstrates the importance of tissue factor as a thrombogenic element in a human whole-vessel model system. TFPI is effective in reducing this thrombogenicity.