Ischemic Postconditioning and Nitric Oxide Administration Failed to Confer Protective Effects in a Porcine Model of Extracorporeal Cardiopulmonary Resuscitation
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Titel:
Ischemic Postconditioning and Nitric Oxide Administration Failed to Confer Protective Effects in a Porcine Model of Extracorporeal Cardiopulmonary Resuscitation
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<jats:title>Abstract</jats:title><jats:p>The protective effects of ischemic postconditioning (<jats:styled-content style="fixed-case">IPC</jats:styled-content>) and nitric oxide (<jats:styled-content style="fixed-case">NO</jats:styled-content>) administration have been demonstrated in several ischemic scenarios. However, current evidence regarding the effect of <jats:styled-content style="fixed-case">IPC</jats:styled-content> and <jats:styled-content style="fixed-case">NO</jats:styled-content> in extracorporeal cardiopulmonary resuscitation remains lacking. Fifteen female swine (body weight 45 kg) underwent veno‐arterial extracorporeal membrane oxygenation (<jats:styled-content style="fixed-case">ECMO</jats:styled-content>) implantation; cardiac arrest‐ventricular fibrillation was induced by rapid ventricular pacing. After 20 min of cardiac arrest, blood flow was restored by increasing the <jats:styled-content style="fixed-case">ECMO</jats:styled-content> flow rate to 4.5 L/min. The animals (five per group) were then randomly assigned to receive <jats:styled-content style="fixed-case">IPC</jats:styled-content> (three cycles of 3 min ischemia and reperfusion), <jats:styled-content style="fixed-case">NO</jats:styled-content> (80 ppm via oxygenator), or mild hypothermia (<jats:styled-content style="fixed-case">HT</jats:styled-content>; 33.0°C). Cerebral oximetry and aortic blood pressure were monitored continuously. After 90 min of reperfusion, blood samples were drawn for the measurement of troponin <jats:styled-content style="fixed-case">I</jats:styled-content>, myoglobin, creatine‐phosphokinase, alanine aminotransferase, neuron‐specific enolase, cystatin <jats:styled-content style="fixed-case">C</jats:styled-content>, and reactive oxygen metabolite (<jats:styled-content style="fixed-case">ROM</jats:styled-content>) levels. Significantly higher blood pressure and cerebral oxygen saturation values were observed in the <jats:styled-content style="fixed-case">HT</jats:styled-content> group compared with the <jats:styled-content style="fixed-case">IPC</jats:styled-content> and <jats:styled-content style="fixed-case">NO</jats:styled-content> groups (<jats:italic>P</jats:italic> < 0.05). The levels of troponin <jats:styled-content style="fixed-case">I</jats:styled-content>, myoglobin, creatine phosphokinase, and alanine aminotransferase were significantly lower in the <jats:styled-content style="fixed-case">HT</jats:styled-content> group (<jats:italic>P</jats:italic> < 0.05); levels of neuron‐specific enolase, cystatin <jats:styled-content style="fixed-case">C</jats:styled-content>, and <jats:styled-content style="fixed-case">ROM</jats:styled-content> were not significantly different. <jats:styled-content style="fixed-case">IPC</jats:styled-content> and <jats:styled-content style="fixed-case">NO</jats:styled-content> were comparable in all monitored parameters. The results of the present study indicate that <jats:styled-content style="fixed-case">IPC</jats:styled-content> and <jats:styled-content style="fixed-case">NO</jats:styled-content> administration are not superior interventions to <jats:styled-content style="fixed-case">HT</jats:styled-content> for the maintenance of blood pressure, cerebral oxygenation, organ protection, and suppression of oxidative stress following extracorporeal cardiopulmonary resuscitation.</jats:p>