The endothelial cell (EC) response during the first 2 h after traumatic hemorrhagic shock (THS) was analyzed in the rat mesentery by electron microscopy. Using a computer-assisted image analysis system, we interactively measured THS-induced changes of the area and the mean height of EC as well as the number of swollen EC occluding the capillary lumen. Analysis distinguished between capillaries presenting with the lumen blocked by corpuscular blood cells and capillaries with an open lumen. THS resulted in a significant increase in EC height of capillaries with an open lumen, but not of capillaries with lumen blocked by blood cells when compared with the control group (p < 0.05). This phenomenon was found to be most prominent 60 min after THS. In addition, THS was accompanied by a significantly increased number of swollen EC which occluded capillaries with an open lumen. From these results we conclude that swelling of EC contributes to THS-induced microvascular injury. Occlusion of the capillary lumen by EC swelling may be regarded as the morphological correlate of the THS-induced ‘no-reflow’ phenomenon.
The aim of this study was to assess early traumatic haemorrhagic shock (THS)-induced changes in myocardial endothelial cells (mECs) both morphologically and morphometrically. The mECs of capillaries of the left ventricular myocardium were investigated by electron microscopy 15, 30, 60, and 120 min after a standardised THS and compared to a control group. With the use of a computer-assisted image analysis system, we measured the following morphometric parameters – height, area, circumference, cytoplasmic processes, and interendothelial junctions – and determined the number and distribution of cytoplasmic vesicles in every mEC. THS induced a significantly increased formation of cytoplasmic processes and a redistribution of cytoplasmic vesicles towards the cell centre, with the changes peaking between 15 and 60 min. There was no evidence of an increase in mEC height or area/circumference ratio used as indicators for early mEC oedema, although the latter dropped significantly after 15 min. No increase in damaged mitochondria was observed and the interendothelial junctions remained close. The THS-induced ultrastructural changes represent early mEC activation. Irreversible damage of mECs does not occur.
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