BACKGROUND: Microcirculatory dysfunctions and mast cell reactions play important roles in hypoxic tissue injuries. The aims of this study were to characterize the effects of hindlimb ischemia-reperfusion on the periosteal microcirculation and to define the consequences of systemic phosphatidylcholine therapy during this condition. MATERIALS AND METHODS: Microcirculatory changes were visualized by means of fluorescence intravital videomicroscopy in anesthetized Wistar rats. 60 min of complete hindlimb ischemia was followed by a 180-min reperfusion in the presence of phosphatidylcholine treatment (50 mg/kg iv; in the second 10 min of reperfusion) or vehicle. Further two groups served as vehicle- or PC-treated sham-operated controls. The proportion of degranulated mast cells and the leukocyte accumulation (myeloperoxidase, MPO assay) were determined in muscle biopsies. RESULTS: Ischemia-reperfusion significantly increased the muscle MPO activity (from 14.94 to 63.45 mU/mg) and the proportion of degranulated mast cells (to 82.5%). The periosteal capillary red blood cell velocity (RBCV) and the functional capillary density (FCD) had decreased, while the primary and secondary leukocyte-endothelial cell interactions had increased by the end of reperfusion (rolling from 20.8 to 40.0%, and firm adherence from 254 to 872 mm-2). Phosphatidylcholine treatment decreased the leukocyte rolling and sticking, preserved the FCD and improved the RBCV The mast cell degranulation and MPO activity diminished significantly in the muscle layer. CONCLUSIONS: Mast cell degranulation accompanies ischemia-reperfusion-induced periosteal microcirculatory derangement. Systemic phosphatidylcholine treatment affords protection through ameliorating secondary inflammatory reactions.
BACKGROUND: Microcirculatory dysfunctions and mast cell reactions play important roles in hypoxic tissue injuries. The aims of this study were to characterize the effects of hindlimb ischemia-reperfusion on the periosteal microcirculation and to define the consequences of systemic phosphatidylcholine therapy during this condition. MATERIALS AND METHODS: Microcirculatory changes were visualized by means of fluorescence intravital videomicroscopy in anesthetized Wistar rats. 60 min of complete hindlimb ischemia was followed by a 180-min reperfusion in the presence of phosphatidylcholine treatment (50 mg/kg iv; in the second 10 min of reperfusion) or vehicle. Further two groups served as vehicle- or PC-treated sham-operated controls. The proportion of degranulated mast cells and the leukocyte accumulation (myeloperoxidase, MPO assay) were determined in muscle biopsies. RESULTS:Ischemia-reperfusion significantly increased the muscle MPO activity (from 14.94 to 63.45 mU/mg) and the proportion of degranulated mast cells (to 82.5%). The periosteal capillary red blood cell velocity (RBCV) and the functional capillary density (FCD) had decreased, while the primary and secondary leukocyte-endothelial cell interactions had increased by the end of reperfusion (rolling from 20.8 to 40.0%, and firm adherence from 254 to 872 mm-2). Phosphatidylcholine treatment decreased the leukocyte rolling and sticking, preserved the FCD and improved the RBCV The mast cell degranulation and MPO activity diminished significantly in the muscle layer. CONCLUSIONS: Mast cell degranulation accompanies ischemia-reperfusion-induced periosteal microcirculatory derangement. Systemic phosphatidylcholine treatment affords protection through ameliorating secondary inflammatory reactions.