Inflammation in Chronic Venous Insufficiency: Is the Problem Insurmountable?

• Published in: Journal of vascular research Vol. 36; no. Suppl 1; pp. 3 - 10
• Main Authors: Takase, Shinya, Delano, Frank A., Lerond, Laurence, Bergan, John J., Schmid-Schönbein, Geert W.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Basel, Switzerland Karger 01.01.1999; S. Karger AG
• Subjects: Animals; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Cell Adhesion; Cell Death; Chronic Disease; Coloring Agents; Constriction; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous; Fluoresceins; Leukocytes - pathology; Leukocytes - physiology; Male; Medical sciences; Mesenteric Veins - physiopathology; Phlebitis - etiology; Propidium; Rats; Rats, Wistar; Reperfusion; Venous Insufficiency - complications; Venous Insufficiency - pathology; Venous Insufficiency - physiopathology; Venous Pressure; Venules - physiopathology; Animal model; Rat; Mesenteric vein; Rodentia; Parenchyma; Cardiovascular disease; Inflammation; Venous incompetence; Flavonoid; Venous disease; Vascular disease; Vertebrata; Chronic; Mammalia; Cell death; Animal; Obliteration
• ISBN: 9783805569330; 3805569335
• ISSN: 1018-1172; 1423-0135
• DOI: 10.1159/000054068

One of the hallmarks of venous insufficiency is an elevated venous pressure. While a number of mechanisms have been proposed for vascular and parenchymal cell damage following venous pressure elevation, such as white cell infiltration, a key question remains as to what degree venous occlusion and flow interruption per se may constitute a risk factor in venous disease. To gain an insight into this mechanism, we examined the effect of venous occlusion followed by reperfusion. A draining venule (circa 50 µm) in the rat mesentery 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 monitored by propidium iodide (PI) labeling. The number of PI-positive cells significantly increased predominantly during reperfusion. A 1-week treatment with a micronized purified flavonoid fraction (100 mg/kg/day) served to significantly reduce parenchymal cell death as well as leukocyte rolling, adhesion to postcapillary venule, and migration into the tissue both during occlusion and reperfusion. The results indicate, that even in an initially symptomless tissue, flow reduction combined with microvascular pressure elevation during venous occlusion results in tissue damage not only during reperfusion (as in arterial occlusion) but also during occlusion.