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血小板减少对兔实验性动脉粥样硬化病变形成的影响。平滑肌细胞增殖和再内皮化。

The effect of thrombocytopenia on experimental arteriosclerotic lesion formation in rabbits. Smooth muscle cell proliferation and re-endothelialization.

作者信息

Friedman R J, Stemerman M B, Wenz B, Moore S, Gauldie J, Gent M, Tiell M L, Spaet H

出版信息

J Clin Invest. 1977 Nov;60(5):1191-201. doi: 10.1172/JCI108872.

DOI:10.1172/JCI108872
PMID:409735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC372473/
Abstract

This study was designed to investigate the mechanisms involved in fibromusculoelastic lesion formation produced by selective de-endothelialization by the intra-arterial balloon catheter technique in thrombocytopenic rabbits. Thrombocytopenia was induced and maintained for up to 30 days by daily injections fo highly specific sheep anti-rabbit platelet sera (APS). Evidence for re-endothelialization was obtained by i.v. Evans blue dye 30 min before sacrifice. Rabbits received daily injections of APS, which reduced the mean platelet count to 5,600/cm3; control animals received identically treated normal sheep sera on the same schedule, and had mean daily platelet counts of 363,000/cm3. Evaluation of intimal thickness was assessed by counting cell layers in semithin sections. Intimal thickening in aortae from rabbits treated with APS was strikingly suppressed, in contrast to those from normal sheep sera-treated animals which showed a mean intimal thickness of 18 cell layers within 28 days often after de-endothelialization. Re-endothelialization was not affected by APS treatment. These results indicate that the proliferation of smooth muscle cells is dramatically inhibited by reduction of platelets.

摘要

本研究旨在探讨在血小板减少的兔中,通过动脉内球囊导管技术进行选择性去内皮化所产生的纤维肌弹性病变形成的相关机制。通过每日注射高特异性羊抗兔血小板血清(APS)诱导并维持血小板减少长达30天。在处死前30分钟经静脉注射伊文思蓝染料以获得再内皮化的证据。兔每日注射APS,其平均血小板计数降至5600/mm³;对照动物按相同方案注射经同样处理的正常羊血清,平均每日血小板计数为363000/mm³。通过计数半薄切片中的细胞层数来评估内膜厚度。与正常羊血清处理的动物相比,接受APS处理的兔主动脉内膜增厚受到显著抑制,正常羊血清处理的动物在去内皮化后28天内平均内膜厚度为18个细胞层。再内皮化不受APS处理的影响。这些结果表明,血小板减少可显著抑制平滑肌细胞的增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/afbe0965859f/jcinvest00659-0237-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/acae1a33c097/jcinvest00659-0234-a.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/d93f482a445b/jcinvest00659-0236-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/883f470733be/jcinvest00659-0236-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/afbe0965859f/jcinvest00659-0237-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/acae1a33c097/jcinvest00659-0234-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/fb74d2e66cb4/jcinvest00659-0235-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/d93f482a445b/jcinvest00659-0236-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/883f470733be/jcinvest00659-0236-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56ce/372473/afbe0965859f/jcinvest00659-0237-a.jpg

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Platelet activation releases megakaryocyte-synthesized apolipoprotein J, a highly abundant protein in atheromatous lesions.血小板活化会释放巨核细胞合成的载脂蛋白J,这是一种在动脉粥样硬化病变中含量很高的蛋白质。
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