BACKGROUND: Microcirculatory dysfunctions and mast cell (MC) reactions play important roles in hypoxic tissue injuries. The aims of this study were to characterize the effects of hindlimb ischemia-reperfusion (I-R) on the periosteal microcirculation and to define the consequences of systemic phosphatidylcholine (PC) therapy during this condition. MATERIALS AND METHODS: Microcirculatory changes were visualized by means of fluorescence intravital videomicroscopy in anesthetized Wistar rats. There was 60 min of complete hindlimb ischemia followed by a 180-min reperfusion in the presence of PC treatment (50 mg/kg i.v.; 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 MCs and the leukocyte accumulation (myeloperoxidase, MPO assay) were determined in muscle biopsies. RESULTS: I-R significantly increased the muscle MPO activity (from 14.94 to 63.45 mU/mg) and the proportion of degranulated MCs (to 82.5%). The periosteal capillary RBC 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)). PC treatment decreased the leukocyte rolling and sticking, preserved the FCD and improved the RBCV. The MC degranulation and MPO activity diminished significantly in the muscle layer. CONCLUSIONS: PC administration improves I-R-induced periosteal microcirculatory dysfunctions and ameliorates secondary inflammatory reactions. Systemic PC treatment could offer a potential treatment modality during hypoperfusion or inflammatory conditions of the bones.
BACKGROUND: Microcirculatory dysfunctions and mast cell (MC) reactions play important roles in hypoxic tissue injuries. The aims of this study were to characterize the effects of hindlimb ischemia-reperfusion (I-R) on the periosteal microcirculation and to define the consequences of systemic phosphatidylcholine (PC) therapy during this condition. MATERIALS AND METHODS: Microcirculatory changes were visualized by means of fluorescence intravital videomicroscopy in anesthetized Wistar rats. There was 60 min of complete hindlimb ischemia followed by a 180-min reperfusion in the presence of PC treatment (50 mg/kg i.v.; 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 MCs and the leukocyte accumulation (myeloperoxidase, MPO assay) were determined in muscle biopsies. RESULTS:I-R significantly increased the muscle MPO activity (from 14.94 to 63.45 mU/mg) and the proportion of degranulated MCs (to 82.5%). The periosteal capillary RBC 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)). PC treatment decreased the leukocyte rolling and sticking, preserved the FCD and improved the RBCV. The MC degranulation and MPO activity diminished significantly in the muscle layer. CONCLUSIONS:PC administration improves I-R-induced periosteal microcirculatory dysfunctions and ameliorates secondary inflammatory reactions. Systemic PC treatment could offer a potential treatment modality during hypoperfusion or inflammatory conditions of the bones.