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Change in endothelial cell shape in response to ischaemia in the cardiac and retinal capillary beds
Author(s) -
Glyn M. C.,
Lawrenson J. G.,
Ward B. J.
Publication year - 2002
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1046/j.1469-7580.2002.00047_11.x
Subject(s) - ischemia , retina , retinal , endothelial stem cell , biology , anatomy , biophysics , cardiology , medicine , biochemistry , neuroscience , in vitro
The change in shape of cardiac capillary endothelial cells in response to ischaemia and ischaemia followed by reperfusion is well established. We investigated the possibility that this process is an active rather than a passive process and that the change might be prevented or attenuated in order to minimise reperfusion injury and ‘no‐reflow’. We have also compared the change in shape of cardiac capillaries with those of the retina. We used an isolated heart preparation in which global ischaemia was induced by cessation of flow. Retinal capillaries were made ischaemic by one of 2 methods, using firstly superfusion with an oxygen depleted medium, and secondly by occlusion of upstream vessels with starch spheres. Ultrastructural and morphometric analysis of cardiac and retinal capillaries demonstrated that the change in shape seen in cardiac capillaries in response to ischaemia does not occur in retinal capillaries reflecting the different metabolic activities of the 2 tissues. Immunocytochemical localisation of _‐actin showed no apparent difference in the retinal capillaries between control and ischaemic capillaries. Cardiac capillaries, however, showed an irregular redistribution of _‐actin in ischaemic vessels which could be attenuated by exposure to phalloidin. Resin casts of ischaemic capillaries showed focal narrowings which were not present in controls. From these results we conclude that the change in endothelial cell shape in response to ischaemia is not a passive process and can be modulated by agents which target the microfilament system.