Inflammation in chronic venous insufficiency: is the problem insurmountable?

One of the hallmarks of venous insufficiency is an elevated venous pressure . While a number of mechanisms have been proposed for vascular and parenchy mal cell damage following venous pressure elevation, such as white cell inf iltration, a key question remains as to what degree venous occlusion and fl ow interruption per se may constitute a risk factor in venous disease. To g ain an insight into this mechanism, we examined the effect of venous occlus ion followed by reperfusion. A draining venule (circa 50 mu m) in the rat m esentery was occluded with a micropipette (1 h) followed by reperfusion (1 h). The procedure serves to raise the microvascular pressure to about 31 mm Hg during the occlusion while the flow is completely stopped in the local venous and capillary network. Parenchymal cell death in the mesentery was m onitored by propidium iodide (PI) labeling. The number of PI-positive cells significantly increased predominantly during reperfusion, A 1-week treatme nt with a micronized purified flavonoid fraction (100 mg/kg/day) served to significantly reduce parenchymal cell death as well as leukocyte rolling, a dhesion to postcapillary venule, and migration into the tissue both during occlusion and reperfusion. The results indicate, that even in an initially symptom less tissue, flow reduction combined with microvascular pressure el evation during venous occlusion results in tissue damage not only during re perfusion (as in arterial occlusion) but also during occlusion.