title: The inflammatory reaction during venous hypertension in the rat.
abstract: OBJECTIVE
  Numerous studies have examined arterial occlusion followed by reperfusion but few studies have reported about venular occlusion which, in contrast to arterial occlusion, is associated with elevation of the capillary blood pressure. Here we examine leukocytes infiltration and tissue injury in rat mesentery during local venular occlusion and venous hypertension followed by reperfusion, and determine the level of protection offered by pretreatment 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 occlusion using a micropipette followed by reperfusion in the rat mesenteric microcirculation pretreated with 0, 50, or 100 mg/kg MPFF for 7 days. Spontaneous leukocyte activation by nitroblue tetrazolium reduction and expression 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, adhesion, and migration as well as parenchymal cell death. These injurious processes were significantly inhibited by MPFF in a those-dependent fashion. MPFF reduced spontaneous leukocyte NBT reduction and the neutropil expression of CD62L, even though CD18 was not affected.
  
  
  CONCLUSIONS
  These results suggested that microvascular occlusion in venules with elevation of the micropressure followed by reperfusion is a highly cytotoxic process in the rat mesentery which can be attenuated by MPFF pretreatment.
authors.affiliation: Department of Bioengineering and Whitaker Institute for Biomedical Engineering, University of California San Diego, La Jolla 92093-0412, USA.
authors.forename: S
authors.initials: S
authors.lastname: Takase
authors.forename: L
authors.initials: L
authors.lastname: Lerond
authors.forename: J J
authors.initials: JJ
authors.lastname: Bergan
authors.forename: G W
authors.initials: GW
authors.lastname: Schmid-Schönbein
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D018821:CD18 Antigens / Q000032:analysis; D016923:Cell Death; D002465:Cell Movement; D004145:Diosmin / Q000627:therapeutic use; D005609:Free Radicals; D006470:Hemorrhage / Q000209:etiology / Q000473:pathology; D006569:Hesperidin / Q000627:therapeutic use; D006973:Hypertension / Q000473:pathology*; D007249:Inflammation; D007511:Ischemia / Q000473:pathology*; D019041:L-Selectin / Q000096:biosynthesis / Q000235:genetics; D007962:Leukocytes / Q000502:physiology*; D008297:Male; D008643:Mesentery / Q000098:blood supply / Q000473:pathology*; D008833:Microcirculation; D009504:Neutrophils / Q000502:physiology; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury / Q000473:pathology* / Q000517:prevention & control; D014689:Venous Insufficiency / Q000473:pathology*; D014699:Venules / Q000473:pathology
chemical_list: D000975:Antioxidants; D018821:CD18 Antigens; D005609:Free Radicals; D017382:Reactive Oxygen Species; D019041:L-Selectin; D004145:Diosmin; D006569:Hesperidin