title: Compartment syndrome-induced microvascular dysfunction: an experimental rodent model.
abstract: BACKGROUND
  Acute compartment syndrome (CS) is a limb-threatening disease that results from increased intracompartmental pressure. The pathophysiologic mechanisms by which this occurs are poorly understood. This study was designed to measure the effects of increased intracompartmental pressure on skeletal muscle microcirculation, inflammation and cellular injury using intravital videomicroscopy (IVVM) in a clinically relevant small animal model.
  
  
  METHODS
  We induced CS in 10 male Wistar rats (175-250 g), using a saline infusion technique. Intracompartmental pressure was controlled between 30 and 40 mm Hg and maintained for 45 minutes. After fasciotomy, the extensor digitorum longus muscle was visualized using IVVM, and perfusion was quantified. We quantified leukocyte recruitment to measure the inflammatory response. We measured muscle cellular injury using a differential fluorescent staining technique.
  
  
  RESULTS
  The number of nonperfused capillaries increased from 12.7 (standard error of the mean [SEM] 1.4 ) per mm in the control group to 30.0 (SEM 6.7) per mm following 45 minutes of elevated intracompartmental pressure (CS group; p = 0.031). The mean number of continuously perfused capillaries (and SEM) decreased from 78.4 (3.2) per mm in the control group to 41.4 (6.9) per mm in the CS group (p = 0.001). The proportion of injured cells increased from 5.0% (SEM 2.1%) in the control group to 16.3% (SEM 6.8%) in the CS group (p = 0.006). The mean number of activated leukocytes increased from 3.6 (SEM 0.7) per 100 μm(2) in the control group to 8.6 (SEM 1.8) per 100 μm(2) in the CS group (p = 0.033).
  
  
  CONCLUSIONS
  Early CS-induced microvascular dysfunction resulted in a decrease in nutritive capillary perfusion and an increase in cellular injury and was associated with a severe acute inflammatory component.
authors: Division of Orthopaedic Surgery, University of Western Ontario, London, Canada. arlawend@uwo.ca
authors: Abdel-Rahman
authors: AR
authors: Lawendy
authors: David W
authors: DW
authors: Sanders
authors: Aurelia
authors: A
authors: Bihari
authors: Neil
authors: N
authors: Parry
authors: Daryl
authors: D
authors: Gray
authors: Amit
authors: A
authors: Badhwar
mesh_terms: D000208:Acute Disease; D000818:Animals; D006690:Bisbenzimidazole; D002196:Capillaries / Q000473:pathology / Q000503:physiopathology*; D003161:Compartment Syndromes / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004996:Ethidium; D005456:Fluorescent Dyes; D007962:Leukocytes; D008297:Male; D008833:Microcirculation; D018715:Microscopy, Video / Q000379:methods; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000293:injuries* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D014657:Vasculitis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*
chemical_list: D005456:Fluorescent Dyes; D004996:Ethidium; D006690:Bisbenzimidazole