PERSISTENT DYSFUNCTION OF REGENERATED ENDOTHELIUM AFTER BALLOON ANGIOPLASTY OF RABBIT ILIAC ARTERY

PERSISTENT DYSFUNCTION OF REGENERATED ENDOTHELIUM AFTER BALLOON ANGIOPLASTY OF RABBIT ILIAC ARTERY
复制标题

DOI:
10.1161/01.cir.81.5.1667
复制
发表时间:
1990-05-01
期刊:
影响因子:
37.8
通讯作者:
COOKE, JP
COOKE, JP
中科院分区:
医学1区
文献类型:
--
作者:
WEIDINGER, FF;MCLENACHAN, JM;COOKE, JP

文献摘要

被引文献

相似文献

本研究探讨了球囊血管成形术后再生的内皮的血管扩张功能,以及这种功能与血管损伤程度和随后的内膜增殖的关系。对47只新西兰白色家兔的左髂动脉进行球囊血管成形术。在“严重”损伤(3.0 mm球囊)或“中度”损伤(2.5 mm球囊)后2周和4周,在体外检查血管反应。两种程度的球囊损伤均导致完全内皮剥脱。两种损伤后2周,组织学证实内皮再生。虽然再生的细胞有不规则的大小和多边形的形状,并缺乏典型的对齐的血流方向,因子VIII相关抗原的免疫细胞化学染色确定这些细胞为内皮。为了研究再生内皮的血管扩张功能,将球囊损伤和对照(对侧)髂动脉的环悬挂在器官室中以记录等长力。严重损伤后2周和4周,球囊损伤血管对乙酰胆碱和钙离子载体A23187的内皮依赖性舒张减少。中度损伤后,这些药物的内皮依赖性舒张在2周时减少,但在4周时恢复正常。然而,在所有研究组中,硝普钠的内皮非依赖性舒张均得以保留。形态计量学分析显示内膜增厚程度与乙酰胆碱的最大舒张作用呈负相关(r = 0.45,P < 0.01)。因此,动脉损伤后受体和非受体介导的内皮依赖性舒张持续减弱。再生的细胞具有改变的形态学外观,但因子VIII相关抗原的染色证实了它们的内皮来源。内皮功能障碍的程度和持续时间取决于初始损伤的严重程度,并与内膜厚度的程度有关。
This study investigated the vasodilator function of endothelium that regenerated after balloon angioplasty and the relation of this function to the extent of vascular injury and to subsequent intimal proliferation. Balloon angioplasty was performed in the left iliac artery of 47 New Zealand White rabbits. Vascular responses were examined in vitro 2 and 4 weeks after a "severe" injury (3.0-mm balloon) or a "moderate" injury (2.5-mm balloon). Both degrees of balloon injury caused complete endothelial denudation. Endothelial regrowth 2 weeks after either injury was confirmed histologically. Although the regenerated cells had irregular sizes and polygonal shapes and lacked the typical alignment in the direction of blood flow, immunocytochemical staining for factor VIII-related antigen identified these cells as endothelium. To study the vasodilator function of regenerated endothelium, rings of balloon-injured and control (contralateral) iliac arteries were suspended in organ chambers for recording of isometric force. Endothelium-dependent relaxation of balloon-injured vessels to acetylcholine and to the calcium ionophore A23187 were reduced at 2 and at 4 weeks after severe injury. After moderate injury, endothelium-dependent relaxations to these agents were reduced at 2 weeks but had normalized by 4 weeks. Endothelium-independent relaxation to sodium nitroprusside, however, was preserved in all study groups. Morphometric analysis revealed an inverse correlation between the degree of intimal thickening and maximal relaxation to acetylcholine (r = 0.45, p < 0.01). Thus, there is a persistent attenuation of receptor- and nonreceptor-mediated endothelium-dependent relaxations after arterial injury. The regenerated cells have an altered morphological appearance, but staining for factor VIII-related antigen confirms their endothelial origin. The degree and duration of endothelial dysfunction depends on the severity of the initial injury and is related to the extent of intimal thickness.