title: The effect of intra-abdominal hypertension incorporating severe acute pancreatitis in a porcine model.
abstract: BACKGROUND
  Abdominal compartment syndrome (ACS) and intra abdominal hypertension(IAH) are common clinical findings in patients with severe acute pancreatitis(SAP). It is thought that an increased intra abdominal pressure(IAP) is associated with poor prognosis in SAP patients. But the detailed effect of IAH/ACS on different organ system is not clear. The aim of this study was to assess the effect of SAP combined with IAH on hemodynamics, systemic oxygenation, and organ damage in a 12 h lasting porcine model.
  
  
  METHODS
  Following baseline registrations, a total of 30 animals were divided into 5 groups (6 animals in each group): SAP+IAP30 group, SAP+IAP20 group, SAP group, IAP30 group(sham-operated but without SAP) and sham-operated group. We used a N(2) pneumoperitoneum to induce different levels of IAH and retrograde intra-ductal infusion of sodium taurocholate to induce SAP. The investigation period was 12 h. Hemodynamic parameters (CO, HR, MAP, CVP), urine output, oxygenation parameters(e.g., S(v)O(2), PO(2), PaCO(2)), peak inspiratory pressure, as well as serum parameters (e.g., ALT, amylase, lactate, creatinine) were recorded. Histological examination of liver, intestine, pancreas, and lung was performed.
  
  
  RESULTS
  Cardiac output significantly decreased in the SAP+IAH animals compared with other groups. Furthermore, AST, creatinine, SUN and lactate showed similar increasing tendency paralleled with profoundly decrease in S(v)O(2). The histopathological analyses also revealed higher grade injury of liver, intestine, pancreas and lung in the SAP+IAH groups. However, few differences were found between the two SAP+IAH groups with different levels of IAP.
  
  
  CONCLUSIONS
  Our newly developed porcine SAP+IAH model demonstrated that there were remarkable effects on global hemodynamics, oxygenation and organ function in response to sustained IAH of 12 h combined with SAP. Moreover, our model should be helpful to study the mechanisms of IAH/ACS-induced exacerbation and to optimize the treatment strategies for counteracting the development of organ dysfunction.
authors.affiliation: Department of General Surgery, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, China.
authors.forename: Lu
authors.initials: L
authors.lastname: Ke
authors.forename: Zhi-hui
authors.initials: ZH
authors.lastname: Tong
authors.forename: Hai-bin
authors.initials: HB
authors.lastname: Ni
authors.forename: Wei-wei
authors.initials: WW
authors.lastname: Ding
authors.forename: Jia-kui
authors.initials: JK
authors.lastname: Sun
authors.forename: Wei-qin
authors.initials: WQ
authors.lastname: Li
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Jie-shou
authors.initials: JS
authors.lastname: Li
mesh_terms: D000208:Acute Disease; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics; D059325:Intra-Abdominal Hypertension / Q000150:complications*; D010100:Oxygen / Q000378:metabolism; D010195:Pancreatitis / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013552:Swine
chemical_list: D010100:Oxygen