Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure.
BACKGROUND
The abdominal compartment syndrome (ACS) has been implicated in the pathogenesis of postinjury multiple organ failure. The ACS is defined as intra-abdominal hypertension causing adverse physiologic response. This study was designed to determine the effects of IAH on the production of interleukin-1b (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and the effects on remote organ injury.


METHODS
IAH was induced in Sprague-Dawley rats which were divided into 5 groups, 10 animals each. Intra-abdominal pressure (IAP) was increased to 20 mm Hg for 60 and 90 minutes in two different groups. In a third group following IAP of 20 mm Hg the abdomen was decompressed for 30 minutes before samples were collected. The other animals were used as controls. Hemodynamic response was monitored throughout the procedure. Cytokine levels were assessed in the plasma. Remote organ injury was assessed by histopathology and myeloperoxidase activity.


RESULTS
IAH caused a significant decrease in MAP. After abdominal decompression MAP returned to baseline levels. A significant decrease in arterial pH was also noted. Increase in the levels of TNF-alpha and IL-6 was noted 30 minutes after abdominal decompression. Plasma concentration of IL-1b was elevated after 60 minutes of IAH. Abdominal decompression, however, did not cause a significant increase in the levels of this cytokine. Lung neutrophil accumulation was significantly elevated only after abdominal decompression. Histopathological findings showed intense pulmonary inflammatory infiltration including atelectasis and alveolar edema.


CONCLUSIONS
IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF.
Rezende-Neto
Joao B
JB
Faculdade de Medicina, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Moore
Ernest E
EE
Melo de Andrade
Marcus Vinicius
MV
Teixeira
Mauro Martins
MM
Lisboa
Felipe Assis
FA
Arantes
Rosa Maria Esteves
RM
de Souza
Danielle Gloria
DG
da Cunha-Melo
Jose Rennan
JR
D000007:Abdominal Injuries / Q000150:complications* / Q000175:diagnosis; D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D001795:Blood Pressure Determination; D003161:Compartment Syndromes / Q000209:etiology / Q000473:pathology; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D006439:Hemodynamics / Q000502:physiology; D006973:Hypertension / Q000150:complications* / Q000175:diagnosis; D018836:Inflammation Mediators / Q000032:analysis*; D007375:Interleukin-1 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D009102:Multiple Organ Failure / Q000209:etiology* / Q000473:pathology*; D011014:Pneumonia / Q000097:blood / Q000473:pathology*; D011336:Probability; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha