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

Abstract:

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 flow 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.

journal_name

Cardiovasc Res

journal_title

Cardiovascular research

authors

Glyn MC,Ward BJ

doi

10.1016/s0008-6363(00)00173-5

subject

Has Abstract

pub_date

2000-11-01 00:00:00

pages

346-56

issue

2

eissn

0008-6363

issn

1755-3245

pii

S0008-6363(00)00173-5

journal_volume

48

pub_type

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