[Mesoglycan and phlebopathy. A clinico-experimental contribution].
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Biomedical subjects
Publications and source records attributed to C Allegra.
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Changes in subcutaneous tissue pressure caused by N2O-He, 1-ATA isobaric counterdiffusion gas phase development were measured. Only the ears of New Zealand White rabbits were subjected to counterdiffusion. The rabbits breathed a mixture of 80% N2O-20% O2 while their ears alone were surrounded by He and the rest of their bodies continued to be surrounded by air. Subcutaneous pressure changes were transmitted to the transducer-recorded system via a fluid-filled subcutaneous needle. When the gas phase developed in subcutaneous tissue, pressure rose and a maximum pressure (Pmax) was reached. Pmax in the counterdiffused ear was 48 +/- 10 (SD) Torr, and mean time to reach Pmax was 75 +/- 10 (SD) min. The findings are discussed in relation to the pathological processes of isobaric inert gas counterdiffusion.
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The effect of a clinically used purified micronized flavonoid fraction (90% diosmin and 10% hesperidin) on leukocyte-endothelial cell interaction during ischemia-reperfusion injury was studied in the microcirculation of unanesthetized hamsters fitted with a skin fold window chamber. The drug was given orally in suspension with arabic gum (30 mg/kg) 8 h prior to induction of 4-hour tourniquet ischemia in the chamber window. Leukocyte-endothelial cell interaction was observed using fluorescence intravital microscopy in postcapillary venules (15-70 microns in diameter) at control and during reperfusion at 30 min and 2 and 24 h. Leukocytes were classified according to their flow pattern as (1) 'passers', including 'free flowing' leukocytes and those which were 'flowing with endothelial contact', and (2) 'immobilized' leukocytes. Untreated animals exhibited a significant increase of 'immobilized' leukocytes and of those 'flowing with endothelial contact' during reperfusion. Flavonoid-treated animals displayed a statistically significant lower number of 'immobilized' leukocytes at all time points during reperfusion. There was no change in the number of leukocytes 'flowing with endothelial contact' relative to the untreated animals. Since firm leukocyte attachment to the endothelial wall and subsequent emigration of leukocytes into the interstitium is a mechanism for tissue damage during inflammation, attenuation of this phenomenon during conditions of ischemia-reperfusion can in part explain previous observations that this purified micronized flavonoid fraction decreases edema formation.