The inflammatory reaction during venous hypertension in the rat

Citation
S. Takase et al., The inflammatory reaction during venous hypertension in the rat, MICROCIRCUL, 7(1), 2000, pp. 41-52
Citations number
54
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
MICROCIRCULATION
ISSN journal
10739688 → ACNP
Volume
7
Issue
1
Year of publication
2000
Pages
41 - 52
Database
ISI
SICI code
1073-9688(200002)7:1<41:TIRDVH>2.0.ZU;2-#
Abstract
Objective: Numerous studies have examined arterial occlusion followed by re perfusion but few studies have reported about venular occlusion which. in c ontrast to arterial occlusion, is associated with elevation of the capillar y blood pressure. Here we examine leukocytes infiltration and tissue injury in rat mesentery during local venular occlusion and venous hypertension fo llowed by reperfusion, and determine the level of protection offered by pre treatment with micronized, purified flavonoid fraction (MPFF). Methods: Leukocyte rolling, adhesion, migration, and parenchymal cell death as detected by propidium iodide labeling were determined during venular oc clusion using a micropipette followed by reperfusion in the rat mesenteric microcirculation pretreated with 0, 50, or 100 mg/kg MPFF for 7 days. Spont aneous leukocyte activation by nitroblue tetrazolium reduction and expressi on of CD18 and CD62L on naive donor neutrophils incubated with plasma from each treatment group were determined. Results: Venous occlusion led to elevated levels of leukocyte rolling, adhe sion, and migration as well as parenchymal cell death. These injurious proc esses were significantly inhibited by MPFF in a dose-dependent fashion. MPF F reduced spontaneous leukocyte NBT reduction and the neutrophil expression of CD62L, even though CD18 was not affected. Conclusion: These results suggested that microvascular occlusion in venules with elevation of the micropressure followed by reperfusion is a highly cy totoxic process in the rat mesentery which can be attenuated by MPFF pretre atment.