[Reproducing and evaluating a rabbit model of multiple organ dysfunction syndrome after cardiopulmonary resuscitation resulted from asphyxia].

OBJECTIVE: To evaluate the reproduction of a model of post resuscitation multiple organ dysfunction syndrome (PR-MODS) after cardiac arrest (CA) in rabbit, in order to provide new methods for post-CA treatment.

METHODS: Thirty-five rabbits were randomly divided into three groups, the sham group (n=5), the 7-minute asphyxia group (n=15), and the 8-minute asphyxia group (n=15). The asphyxia CA model was reproduced with tracheal occlusion. After cardiopulmonary resuscitation (CPR), the ratio of recovery of spontaneous circulation (ROSC), the mortality at different time points and the incidence of systemic inflammatory response syndrome (SIRS) were observed in two asphyxia groups. Creatine kinase isoenzyme (CK-MB), alanine aminotransferase (ALT), creatinine (Cr), glucose (Glu) and arterial partial pressure of oxygen (PaO2) levels in blood were measured in the two asphyxia groups before CPR and 12, 24 and 48 hours after ROSC. The survived rabbits were euthanized at 48 hours after ROSC, and heart, brain, lung, kidney, liver, and intestine were harvested for pathological examination using light microscope. PR-MODS after CA was defined based on the function of main organs and their pathological changes.

RESULTS: (1) The incidence of ROSC was 100.0% in 7-minute asphyxia group and 86.7% in 8-minute asphyxia group respectively (P>0.05). The 6-hour mortality in 8-minute asphyxia group was significantly higher than that in 7-minute asphyxia group (46.7% vs. 6.7%, P<0.05), and the mortality of 8-minute asphyxia group at 12 - 48 hours was slightly higher compared with that of 7-minute asphyxia group (all P>0.05). (2) There was a variety of organ dysfunctions in survived rabbits after ROSC, including chemosis, respiratory distress, hypotension, abdominal distension, weakened or disappearance of bowel peristalsis and oliguria. (3) There was no SIRS or associated changes in major organ function in the sham group. SIRS was observed at 12 - 24 hours after ROSC in the two asphyxia groups. CK-MB was increased significantly at 12 hours after ROSC compared with that before asphyxia (7-minute asphyxia group: 786.88±211.84 U/L vs. 468.20±149.45 U/L, 8-minute asphyxia group: 894.88±248.80 U/L vs. 462.11±115.15 U/L, both P<0.05), ALT, Cr and Glu were elevated obviously at 24 hours after ROSC (7-minute asphyxia group ALT: 174.25±36.28 U/L vs. 50.27±9.37 U/L, Cr: 144.25±41.64 μmol/L vs. 67.71±16.47 μmol/L, Glu: 11.21±1.14 mmol/L vs. 5.59±1.10 mmol/L; 8-minute asphyxia group ALT: 205.50±10.61 U/L vs. 51.13±10.37 U/L, Cr: 230.50±88.39 μmol/L vs. 65.93±13.81 μmol/L, Glu: 11.55±0.35 mmol/L vs. 6.41±1.23 mmol/L, all P<0.05), and PaO2 was lowered significantly at 48 hours after ROSC (7-minute asphyxia group: 5.03±0.73 kPa vs. 9.07±1.03 kPa, P<0.05). (4) There were pathological changes in major organ in the survived rabbits at 48 hours after ROSC (only 4 rabbits survived in 7-minute asphyxia group), including infiltration of inflammatory cells, partial cellular degeneration, edema, necrosis and tissue bleeding in major organs.

CONCLUSION: If the SIRS and dysfunction of two or more organ were defined in animals after ROSC, the signs, biochemical markers and nonspecific pathological changes could be accepted to evaluate the PR-MODS.