Extracorporeal Life Support Increases Survival After Prolonged Ventricular Fibrillation Cardiac Arrest in the Rat

Abstract

Background:Extracorporeal life support (ECLS) for cardiopulmonary resuscitation (CPR) may increase end organ perfusion and thus survival when conventional CPR fails. The aim was to investigate, if after ventricular fibrillation cardiac arrest in rodents ECLS improves outcome compared with conventional CPR.Methods:In 24 adult male Sprague–Dawley rats (460–510 g) resuscitation was started after 10 min of no-flow with ECLS (consisting of an open reservoir, roller pump, and membrane oxygenator, connected to cannulas in the jugular vein and femoral artery, n = 8) or CPR (mechanical chest compressions plus ventilations, n = 8) and compared with a sham group (n = 8). After return of spontaneous circulation (ROSC), all rats were maintained at 33°C for 12 h. Survival to 14 days, neurologic deficit scores and overall performance categories were assessed.Results:ECLS leads to sustained ROSC in 8 of 8 (100%) and neurological intact survival to 14 days in 7 of 8 rats (88%), compared with 5 of 8 (63%) and 1 of 8 CPR rats. The median survival time was 14 days (IQR: 14–14) in the ECLS and 1 day (IQR: 0 to 5) for the CPR group (P = 0.004).Conclusion:In a rat model of prolonged ventricular fibrillation cardiac arrest, ECLS with mild hypothermia produces 100% resuscitability and 88% long-term survival, significantly better than conventional CPR.

Comparison of the effect of membrane sizes and fibre arrangements of two membrane oxygenators on the inflammatory response, oxygenation and decarboxylation in a rat model of extracorporeal membrane oxygenation

“…Magnet et al used the SAMO in a rat model of cardiac arrest. After 15 min of ECMO with a blood flow of 100 ml/kg/min and a FiO 2 of 1.0, they measured a pO 2 of 443 mmHg, which is similar to that in our findings [13]. The Micro-1 oxygenator was validated in a rat model of CPB by Dong et al [8].…”

“…In the past, both oxygenators have been used in different rat models, including models of CPB and deep hypothermic cardiac arrest (DHCA) [8,9,[12][13][14][15]17]. To the best of our knowledge, they have not been compared regarding their oxygenation, decarboxylation, dilutional anaemia and inflammation response to date.…”

“…Further, the pCO 2 was adjusted by the sweep gas flow over the membrane, which explained that the pCO 2 was reported between 35 and 45 mmHg in previous studies [8,13,17].…”

“…In contrast, the small animal membrane oxygenator (SAMO, M. Humbs, Valley, Germany) consists of a three-layered hollow-fibre membrane with a gas exchange area of 500 cm 2 and a priming volume of 7 ml [9]. Both oxygenators have been used successfully in different models [8][9][10][11][12][13][14][15]. Models without a requirement for blood transfusion offer the opportunity to measure the extracorporeal oxygenation-induced inflammatory response.…”

Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis

“…Rats were observed every 2 h within first 24 h after ROSC. Then rats were observed at 48 and 72 h. During the 72-h observation period, gasping or respiratory rate under 5 breaths/min required immediate euthanasia ( 29 ). At 72 h, all surviving rats were re-anesthetized with 5% isoflurane and had a vein catheter placed for blood sampling.…”