title: A mouse model for evaluation of capillary perfusion, microvascular permeability, cortical blood flow, and cortical edema in the traumatized brain.
abstract: Genetically engineered mice have successfully been used to investigate molecular and cellular mechanisms associated with cell dysfunction following brain trauma. Such animals may also offer a possibility to investigate mechanisms involved in posttraumatic hemodynamic alterations. The objective of the study was to establish a mouse model in which important hemodynamic alterations following trauma could be analyzed. C57/BL6 male mice were subjected to controlled cortical impact injury (CCI) or sham-injury. Distribution of blood flow was estimated by determining number of perfused capillaries using FITC-dextran as an intravascular marker. Cortical blood flow was measured using [(14)C]-iodoantipyrine, brain water content (BWC) was measured using a wet vs. dry weight method, and permeability surface area product (PS) was estimated by the transfer constant for [(51)Cr]-EDTA. Number of perfused capillaries in the contusion area was progressively reduced during the first 24 h following trauma by at most 60% relative to a value of 329 +/- 61/mm(2) in sham-injured animals. Blood flow in the contusion area decreased simultaneously by at most 50% relative to a control value of 1.8 +/- 0.4 mL.min(-1).g(-1), and was reduced further in subregions within the contusion area. BWC in the injured hemisphere increased from 79.3 +/- 0.5% at control to at most 79.9 +/- 0.6% at 24 h post trauma. PS in the injured hemisphere increased by 71% at 3 h post trauma relative to a control value of 0.45 +/- 0.1 microL.min(-1).g(-1), and was close to control at 24 h. The present study demonstrates that brain trauma in addition to a reduction in cortical blood flow, reduces number of perfused capillaries, which most likely affects exchange of nutrients and fluid. The CCI in mouse is likely to be a useful tool to elucidate mechanisms involved in hemodynamic alterations following brain trauma.
authors.affiliation: Department of Physiological Sciences, University of Lund and Lund University Hospital, Lund, Sweden. Cornelia.Lundblad@mphy.lu.se
authors.forename: C
authors.initials: C
authors.lastname: Lundblad
authors.forename: P O
authors.initials: PO
authors.lastname: Grände
authors.forename: P
authors.initials: P
authors.lastname: Bentzer
mesh_terms: D000818:Animals; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology; D002196:Capillaries / Q000503:physiopathology; D002199:Capillary Permeability / Q000502:physiology*; D002540:Cerebral Cortex / Q000098:blood supply / Q000293:injuries* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D045604:Extracellular Fluid / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL