A New Model for the Study of the Abdominal Compartment Syndrome in Rats

Background The purpose of the present study was to develop of a rodent model of abdominal compartment syndrome (ACS), which allows detailed analysis of intra-abdominal hypertension (IAH)- and decompression-associated reperfusion injury. Methods In 20 anesthetized and ventilated Sprague-Dawley rats a...

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Bibliographic Details
Published in:The Journal of surgical research 2007-05, Vol.139 (2), p.209-216
Main Authors: Meier, Christoph, M.D, Contaldo, Claudio, M.D, Schramm, René, Ph.D, Holstein, Joerg H., M.D, Hamacher, Juerg, M.D, Amon, Michaela, M.D, Wanner, Guido, M.D, Trentz, Otmar, M.D, Menger, Michael D., M.D
Format: Article
Language:English
Subjects:
Abdomen - blood supply
abdominal compartment syndrome
Animals
Arterial hypertension. Arterial hypotension
Arteries
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure
Body Fluids - metabolism
Body Weight
Carbon Dioxide - blood
Cardiology. Vascular system
Central Venous Pressure
Compartment Syndromes - complications
Compartment Syndromes - pathology
Compartment Syndromes - physiopathology
Compartment Syndromes - surgery
Decompression, Surgical
Disease Models, Animal
Female
General aspects
Hypertension - etiology
intra-abdominal hypertension
intra-abdominal pressure
Liver - pathology
Male
Medical sciences
multiorgan dysfunction syndrome
Oxygen - blood
rat model
Rats
Rats, Sprague-Dawley
Reperfusion Injury
Reproducibility of Results
Surgery
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Summary:Background The purpose of the present study was to develop of a rodent model of abdominal compartment syndrome (ACS), which allows detailed analysis of intra-abdominal hypertension (IAH)- and decompression-associated reperfusion injury. Methods In 20 anesthetized and ventilated Sprague-Dawley rats an IAH of 20 mmHg was induced for 3 h by intraperitoneal infusion of gelatin polysuccinate. After decompression, an additional 3-h period of reperfusion was studied. Sham-operated animals, undergoing identical procedures without IAH induction, served as controls. Controlled hyperventilation and intravenous fluid substitution were adapted to keep PCO2 100 mmHg. Results IAH of 20 mmHg could successfully be maintained for the entire 3-h period. MAP was not affected during IAH, however, decreased upon decompression despite forced fluid resuscitation. CVP was markedly elevated during IAH, but returned to baseline after decompression. Of interest, the IAH-induced reduction of PaO2 did not recover to baseline after decompression, indicating a persistent deterioration of gas exchange. In contrast, IAH-associated elevation of PaCO2 normalized during reperfusion. IAH was further accompanied by metabolic acidosis, which persisted after decompression, indicating reperfusion injury. IAH was further associated with a significant increase of serum potassium, lactate, AST, LDH, bilirubin, urea, and creatinine as well as creatine kinase (CK) and CK-MB. Histomorphological analysis revealed parenchymal injury in liver, lung, intestine, and myocardium. Conclusion We established an easily reproducible ACS model in the rat, demonstrating hemodynamic deteriorations and organ dysfunctions similar as known from patients with IAH. Decompression did not restore functional deteriorations, indicating persistent post-ACS reperfusion injury. The model may be suitable to study mechanisms and novel treatment strategies in ACS.
ISSN:0022-4804
1095-8673
DOI:10.1016/j.jss.2006.08.002