Abstract
To explore the effects of different asphyxia time on the reproduction of multiply organ dysfunction syndrome in rabbit after cardiopulmonary resuscitation (CPR-MODS) for cardiac arrest, in order to provide a method to reproduce an animal model of CPR-MODS for further research of cardiopulmonary resuscitation (CPR). The rabbit cardiac arrest was caused by asphyxia as a result of clamping the trachea. Thirty rabbits were divided into 7-minute asphyxia group and 8-minute asphyxia group by means of random number table with 15 rabbits in each group. The rate of resumption of spontaneous circulation (ROSC), the mortality at different time points and the occurrence incidence of systemic inflammatory response syndrome (SIRS) of two groups were observed after CPR and the ROSC. The levels of serum tumor necrosis factor-α (TNF-α), myocardial MB-isoenzyme of creatine kinase (CK-MB), alanine aminotransferase (ALT), creatinine (Cr), glucose (Glu) and arterial partial pressure of oxygen (PaO₂) before resuscitation and 12, 24 and 48 hours after ROSC were measured simultaneously in the two groups. The incidence of CPR-MODS was calculated. The CPR time (seconds) in 7-minute asphyxia group was significantly shorter than that in 8-minute asphyxia group (147.60±22.09 vs. 193.08±23.07, P<0.01). The ROSC rate of 7-minute asphyxia group and 8-minute asphyxia group was 100.00% and 86.67%, respectively, and there was no significant difference. The incidence of MODS in the rabbits surviving more than 24 hours after ROSC was 100% in both groups. The mortality at 6 hours after ROSC in 7-minute asphyxia group was remarkably lower than that of 8-minute asphyxia group (6.67% vs. 46.67%, P<0.05). All the rabbits in 8-minute asphyxia group died at 48 hours. The incidence of SIRS after ROSC was 100% in both groups. Compared with that before asphyxiation, the level of serum TNF-α (ng/L) as well as CK-MB (U/L) increased significantly at 12 hours after ROSC in both groups (TNF-α in 7-minute asphyxia group: 100.71±20.43 vs. 49.13±8.64, in 8-minute asphyxia group: 118.09±21.90 vs. 48.48±6.70; CK-MB in 7-minute asphyxia group: 786.88±211.84 vs. 468.20±149.45, in 8-minute asphyxia group: 894.88±248.80 vs. 462.11±115.15, all P<0.05). There was a significant elevation of ALT (U/L) and Glu (mmol/L) at 24 hours after ROSC (ALT in 7-minute asphyxia group: 174.25±36.28 vs. 50.27±9.37, in 8-minute asphyxia group: 205.50±10.61 vs. 51.13±10.37; Glu in 7-minute asphyxia group: 11.21±1.14 vs. 5.59±1.10, in 8-minute asphyxia group: 11.55±0.35 vs. 6.41±1.23, all P<0.05). Cr (μmol/L) was significantly higher at 12 hours after ROSC in 8-minute asphyxia group (98.83±16.70 vs. 65.93±13.81), while it was elevated at 24 hours in 7-minute asphyxia group (144.25±41.64 vs. 67.71±16.47, both P<0.05). PaO₂ in both groups was significantly higher at 12 hours after ROSC and significantly decreased at 24 hours. The model of cardiac arrest caused by 7 minutes asphyxia provided more possibility and feasibility for the subsequent study of reproducing CPR-MODS model.
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