title: Leukocyte migration in the leg in response to experimental venous hypertension.
abstract: OBJECTIVE
  Leukocyte trapping and activation in the microcirculation of the legs may play an important role in causing skin damage in venous disease. Leukocyte emigration from the microcirculation and subsequent locomotion in response to venous hypertension was studied in a group of 12 normal volunteers using a "skin window" technique.
  
  
  METHODS
  Two 0.5-cm square dermal abrasions were made with a dental stone over the gaiter area of the leg and the flexor aspect of the forearm (control), which were covered with moist micropore membranes. The volunteers lay supine for 30 minutes, and then stood supported for 30 minutes to raise the venous pressure in the leg, and then lay supine again for 30 minutes. The experiment was repeated in six volunteers who lay supine for the whole period. The membranes were changed and collected every 15 minutes, fixed in formal saline solution, and dual-stained for monocytes and polymorphonuclear leukocytes. The type and numbers of cells that emigrated and the furthest distance traveled (leading front) by the cells through the membrane were measured.
  
  
  RESULTS
  Both in arms and legs, the vast majority of cells that emigrated were neutrophils, with very few monocytes (arm, 93% neutrophils and 7% monocytes; leg, 97% neutrophils and 3% monocytes). In the 30 minutes after venous hypertension, leukocyte migration significantly decreased in the leg (median leukocyte locomotion: basal, 75.3 microns; standing, 73.5 microns; after hypertension, 62.9 microns; p = 0.012, Wilcoxon matched pairs signed rank test), but not in the arm (basal, 86.2 microns; standing, 84.4 microns; after hypertension, 85.5 microns; p = NS) or when the experiment was repeated with the volunteers lying supine for the entire period (basal, 91.5 microns; standing, 89.4 microns; after hypertension, 92.6 microns; p = NS).
  
  
  CONCLUSIONS
  Leukocyte migration is decreased immediately after experimental venous hypertension, which may be a result of the release of factors that inhibit migration.
authors.affiliation: Department of Surgery, University College London Medical School, UK.
authors.forename: M
authors.initials: M
authors.lastname: Saharay
authors.forename: I E
authors.initials: IE
authors.lastname: Addison
authors.forename: D A
authors.initials: DA
authors.lastname: Shields
authors.forename: J H
authors.initials: JH
authors.lastname: Scurr
authors.forename: P D
authors.initials: PD
authors.lastname: Smith
mesh_terms: D000328:Adult; D002465:Cell Movement / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007866:Leg / Q000098:blood supply*; D007962:Leukocytes / Q000502:physiology*; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D008851:Micropore Filters; D008875:Middle Aged; D011187:Posture / Q000502:physiology; D012016:Reference Values; D012884:Skin Window Technique; D013997:Time Factors; D014680:Veins