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Original Articles
NUMBER 3-4 YEAR 2011
An Improved Model of Severe Sepsis in Pigs
1 Institute of Surgical Research, University of Szeged, Hungary,
2 Pius Branzeu Center for Microsurgery and Laparoscopic Surgery, Victor Babes University of Medicine and Pharmacy, Timisoara,
3 Department of Medical Microbiology and Immunobiology, University of Szeged, Hungary

Correspondence to:
Mihály Boros MD, PhD, DSc, Institute of Surgical Research, University of Szeged,
PO Box 427, H-6701 Szeged, Hungary,
Tel: +36-62-545103
Obiectiv: Dezvoltarea unui model de studiu al sepsei pe animalul mare de laborator prin inducerea peritonitei fecale, cu reproducerea caracteristicilor macrohemodinamice, microcirculatorii si inflamatorii, obiectivate in sepsa umana incipienta. Material si metode: Porcii pitici anesteziati au fost supusi peritonitei fecale (n = 9; 0,5 g/kg i.p., autofecale) sau operatiei-control (ser fiziologic i.p., n = 6). Gazimetria a fost monitorizata hemodinamic invaziv la 15-24 ore postchirurgical. Microcirculatia sublinguala a fost exprimata prin modificarile velocitatii eritrocitare (MVE) (prin imagistica spectrala a polarizarii octogonale), in timp ce intervalul PCO2 intestinal a fost masurat prin tonometrie indirecta. Nivelele plasmatice ale proteinei HMGB1 si oxidului nitric/nitrat (NOx) au fost determinate din probe de sange venos. Rezultate: Presiunea arteriala medie a scazut treptat sub 70 mm Hg la animalele cu sepsis, in timp ce frecventa cardiaca si debitul cardiac au crescut constant. In ciuda reactiilor hiperdinamice, MVE a scazut, in timp ce intervalul PCO2 a crescut semnificativ, in comparatie cu grupul control. Concentratiile plasmatice ale NOx si HMGB1 au fost semnificativ crescute la 6-16 ore de la debutul peritonitei. Concluzii: Raportam dezvoltarea unui nou model experimental de studiu al sepsei prin inducerea peritonite fecale la animalul de laborator. Datele obtinute in vivo sugereaza ca acest model experimental este relevant clinic si poate avea un rol inovator in dezvoltarea terapiilor anti-sepsa.

Objective: Our aim was to develop a large animal model of sepsis, induced by fecal peritonitis, which reproduces the characteristic macrohemodynamic, microcirculatory and inflammatory changes seen in early human sepsis. Material and methods: Anesthetized minipigs were subjected to fecal peritonitis (n = 9; 0.5 g/kg i.p. autofeces) or sham-operation (i.p. saline, n = 6). Invasive hemodynamic monitoring was started with regular blood gas analyses between the 15-24 hr of the insult. Sublingual microcirculation was characterized by red blood cell velocity (RBCV) changes (with orthogonal polarization spectral imaging), while the intestinal PCO2 gap was measured by indirect tonometry. The plasma levels of high mobility group box protein 1 (HMGB1) and nitrite/nitrate (NOx) were determined from venous blood samples. Results: The mean arterial pressure gradually decreased below 70 mm Hg in septic animals, while the heart rate and cardiac output increased constantly. In spite of the hyperdynamic reaction the sublingual RBCV decreased, while intestinal PCO2 gap increased significantly as compared with the control group. The NOx and HMGB1 plasma concentrations were significantly elevated between 6-16 hr of peritonitis. Conclusion: We report on the introduction of a new animal model fecal peritonitis-induced sepsis. The in vivo data suggest that this experimental model is of clinical relevance and may play useful roles in the development of novel, sepsis-related therapies.

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