title: Microvascular response to shock wave application in striated skin muscle.
abstract: BACKGROUND
  This study aims to quantify by intravital microscopy the microhemodynamic response after extracorporeal shock wave application (ESWA) to the physiologic microcirculation of the mouse dorsal skinfold chamber.
  
  
  METHODS
  ESWA was carried out using an electrohydraulic shock wave source. Two different shock wave doses of 500 and 1000 pulses at an energy flux rate of 0.08 mJ/mm(2) and a frequency of 4 Hz were compared with sham-operated animals. Microcirculatory analyses were performed at baseline (BL) and during a 3 d observation period after ESWA. The expression of caspase-3 (casp-3), proliferating cell nuclear antibody (PCNA), von Willebrand factor (vWF), and endothelial nitric oxide synthase (eNOS) were analyzed semiquantitatively by immunohistochemistry.
  
  
  RESULTS
  ESWA provoked a significant and persistent increase of functional capillary density (FCD) throughout the observation period, reaching a maximum (140% ± 5% of BL, P < 0.05 versus sham) after 1 d when animals were treated with 1000 pulses. ESWA induced a slight increase of leukocyte rolling (∼2- to ∼3.5-fold, P < 0.05) and leukocyte adherence (∼1.5- to ∼2-fold, P < 0.05) to the endothelial lining of postcapillary venules. One day following ESWA, we observed enhanced expression of casp-3 (∼3- to ∼4-fold), PCNA (∼9- to ∼14-fold), vWF (∼11- to ∼14-fold), and eNOS (∼3-fold), all P < 0.05.
  
  
  CONCLUSIONS
  This study shows that ESWA provokes a favorable persistent increase of patent capillaries, however accompanied by a transient and slight inflammatory response but also by dose-dependant apoptotic cell death. Our data suggest that ESWA might represent a noninvasive biomechanical tool to treat critically perfused and endangered tissues, but certainly warrants further investigation.
authors.affiliation: Department of Surgery, Division of Plastic and Reconstructive Surgery, University Hospital Zurich, Zurich, Switzerland.
authors.forename: Maurizio
authors.initials: M
authors.lastname: Calcagni
authors.forename: Fanfan
authors.initials: F
authors.lastname: Chen
authors.forename: Dominik C
authors.initials: DC
authors.lastname: Högger
authors.forename: Nicole
authors.initials: N
authors.lastname: Lindenblatt
authors.forename: Marius
authors.initials: M
authors.lastname: Keel
authors.forename: Pietro
authors.initials: P
authors.lastname: Giovanoli
authors.forename: Claudio
authors.initials: C
authors.lastname: Contaldo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001160:Arterioles / Q000502:physiology; D053148:Caspase 3 / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology / Q000502:physiology; D007962:Leukocytes / Q000502:physiology; D008096:Lithotripsy; D051379:Mice; D008810:Mice, Inbred C57BL; D008833:Microcirculation / Q000502:physiology*; D054792:Muscle, Striated / Q000098:blood supply*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D012867:Skin / Q000098:blood supply*; D014699:Venules / Q000502:physiology; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D014841:von Willebrand Factor; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse; C505409:Casp3 protein, mouse; D053148:Caspase 3