In vivo visualization of nitric oxide and interactions among platelets, leukocytes, and endothelium following hemorrhagic shock and reperfusion
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We examined changes in nitric oxide (NO) distribution in the mesenteric microcirculation after hemorrhagic shock and reperfusion (H/R), and correlated NO production to leukocyte and platelet behavior.
Materials and methods
The behavior of leukocytes and platelets in mesenteric venules was observed by intravital microscopy at 0.5 and 24 h after H/R in male Wistar rats. Transvascular leakage of fluorescein isothiocyanate-labeled albumin was assessed by epi-illumination. The NO-sensitive dye, 4,5-diaminofluorescein diacetate, was used for imaging NO release.
H/R significantly increased vascular albumin leakage and adhesion of leukocytes and platelets (P < 0.05). In H/R 0.5 h rats, NO production in the venular endothelium declined. However, NO production was elevated in H/R 24 h rats in mast cells (P < 0.05). Leukocyte adherence, platelet adherence, and venular permeability were attenuated by iNOS inhibition.
Mesenteric endothelial cell dysfunction after H/R 0.5 h is associated with reduced NO, whereas after H/R 24 h is related to increase NO in mast cells.