title: Prostacyclin reduces plasma volume loss after skeletal muscle trauma in the rat.
abstract: BACKGROUND
  Trauma induces transcapillary leakage of fluid and proteins because of increased microvascular permeability. Based on studies showing that prostacyclin (PGI2) has permeability-reducing properties, in the present study, we investigated whether PGI2 reduces plasma volume (PV) loss after a nonhemorrhagic trauma.
  
  
  METHODS
  The study was performed on anesthetized Sprague-Dawley rats exposed to a controlled standardized blunt trauma to the abdominal rectus muscle. Thereafter, the animals were randomized to treatment with either PGI2 (2 ng/kg per minute) or 0.9% NaCl. PV was estimated before and 3 hours after the trauma using I-albumin as tracer. In separate experiments, the transcapillary escape rate of I-albumin was calculated and plasma concentrations of cytokines were measured after both treatments.
  
  
  RESULTS
  Average PV at baseline was 41.6 mL/kg ± 2.5 mL/kg and 42.3 mL/kg ± 1.7 mL/kg in the PGI2 and NaCl animals, respectively. PV was decreased by 22% ± 8% in the NaCl animals and by 11% ± 9% in the PGI2 animals 3 hours after the trauma (p < 0.05). Trauma induced a decrease in mean arterial blood pressure and an increase in hematocrit in both groups. There were no differences in urine production and mean arterial blood pressure between the PGI2 and NaCl animals. The transcapillary escape rate for albumin was calculated for one hour starting 30 minutes after the trauma and was 15.1% ± 2.4% per hour in the PGI2 animals and 17.4% ± 3.3% per hour in the NaCl animals (p = 0.09). Interleukin 6 concentration 3 hours after the trauma was lower in the PGI2 animals than in the NaCl animals (p < 0.05).
  
  
  CONCLUSIONS
  We conclude that PGI2 attenuates PV loss after blunt muscle trauma. The vascular effects of PGI2 are associated with a modulation of the trauma-induced inflammatory response.
authors.affiliation: Department of Anesthesia and Intensive Care, Lund University and Skåne University Hospital, Lund, Sweden. peter.bansch@med.lu.se
authors.forename: Peter
authors.initials: P
authors.lastname: Bansch
authors.forename: Cornelia
authors.initials: C
authors.lastname: Lundblad
authors.forename: Per-Olof
authors.initials: PO
authors.lastname: Grände
authors.forename: Peter
authors.initials: P
authors.lastname: Bentzer
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology; D011464:Epoprostenol / Q000627:therapeutic use*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D018482:Muscle, Skeletal / Q000293:injuries* / Q000503:physiopathology; D010953:Plasma Volume / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014665:Vasodilator Agents / Q000627:therapeutic use*; D014949:Wounds, Nonpenetrating / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D015850:Interleukin-6; D014665:Vasodilator Agents; D016753:Interleukin-10; D011464:Epoprostenol