Blocking of endothelial-leukocyte interaction (rolling) does not improve reflow in the rat gastric mucosa after hemorrhagic shock and retransfusion.
The polymorphonuclear neutrophilic granulocyte (PMN) has been implicated as one possible cause of the no-reflow phenomenon seen upon reperfusion after ischemia, by, for instance, the release of toxic substances and/or microvascular flow obstruction. In the present study we studied the effects of ascorbate (an antioxidant) and fucoidin (an inhibitor of leukocyte rolling in microvessels) on the rat gastric mucosal and submucosal PMN content and vascular patency (the latter assessed as the surface density of perfused vessels) in connection with hemorrhagic shock (15 min) and retransfusion (5 or 10 min). The effect of fucoidin on the leukocyte rolling in small venules was studied separately with vital microscopy in the rat mesentery. As found in earlier studies, shock and retransfusion led to a decrease in the surface density of perfused vessels, whereas the number of PMNs in the mucosa or the submucosa was not affected by shock and retransfusion. Ascorbate improved vascular patency without affecting the PMN content. In the mesentery, fucoidin caused a 76% reduction in the number of rolling PMNs and it reduced significantly the number of PMNs in the mucosa, but not in the submucosa, after 10 min of retransfusion. Fucoidin had no effect on the vascular patency at that or any other time point. On the basis of these experiments it is concluded that PMN accumulation cannot be singled out as the cause of no-reflow in the rat gastric mucosa after shock and retransfusion of the degree and duration analyzed in this investigation.[1]References
- Blocking of endothelial-leukocyte interaction (rolling) does not improve reflow in the rat gastric mucosa after hemorrhagic shock and retransfusion. Ekman, T., Risberg, B., Bagge, U., Braide, M. Shock (1994) [Pubmed]
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