Contraction in cardiac endothelial cells contributes to changes in capillary dimensions following ischaemia and reperfusion

被引:18
作者
Glyn, MCP [1 ]
Ward, BJ [1 ]
机构
[1] Univ London Queen Mary & Westfield Coll, London E1 4NS, England
关键词
capillaries; contractile apparatus; contractile function; electron microscopy; endothelial function; ischaemia-reperfusion;
D O I
10.1016/S0008-6363(00)00173-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: Ischaemia followed by reperfusion brings about a reduction in cardiac capillary cross-sectional dimensions which is consistent with constriction. The aim of this study was to test the hypothesis that the reduction in cardiac capillary dimensions that occurs in ischaemia and reperfusion is caused by endothelial cell contraction and that modulating the endothelial cell contractile apparatus reduces microvascular reperfusion injury. Methods: In isolated rat hearts we used phalloidin to stabilise the endothelial actin filaments in order to prevent the dimensional changes during ischaemia. The changes in endothelial cell dimensions were quantified by measuring whole capillary and luminal cross-sectional areas. abluminal and luminal membrane lengths. We have also used resin casts of the coronary vasculature coupled with scanning electron microscopy to examine the structural changes along the length of the capillaries in ischaemia-reperfusion. Results: We found that the reduction in capillary dimensions was prevented by the addition of phalloidin and, in the resin casts, that ischaemia-reperfusion cause focal narrowings along the capillaries which are consistent with constriction. Conclusions: (1)The endothelial contractile apparatus is involved in the reduction in cross-sectional dimensions. (2) This implies that the capillary bed may have a greater role in the local control of how than was previously thought and that modulation of the actomyosin contractile system in cardiac capillary endothelial cells may be useful in reducing 'no reflow' injury which results from reperfusion. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:346 / 356
页数:11
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