Abstract
IntroductionInhaled nitric oxide (iNO) improves outcomes when given post systemic ischemia/reperfusion injury. iNO given during cardiopulmonary resuscitation (CPR) may therefore improve return of spontaneous circulation (ROSC) rates and functional outcome after cardiac arrest (CA).MethodsThirty male Sprague-Dawley rats were subjected to 10 minutes of CA and at least 3 minutes of CPR. Animals were randomized to receive either 0 (n = 10, Control), 20 (n = 10, 20 ppm), or 40 (n = 10, 40 ppm) ppm iNO during CPR until 30 minutes after ROSC. A neurological deficit score was assessed daily for seven days following the experiment. On day 7, brains, hearts, and blood were sampled for histological and biochemical evaluation.ResultsDuring CPR, 20 ppm iNO significantly increased diastolic arterial pressure (Control: 57 ± 5.04 mmHg; 20 ppm: 71.57 ± 57.3 mmHg, p < 0.046) and decreased time to ROSC (Control: 842 ± 21 s; 20 ppm: 792 ± 5 s, (p = 0.02)).Thirty minutes following ROSC, 20 ppm iNO resulted in an increase in mean arterial pressure (Control: 83 ± 4 mmHg; 20 ppm: 98 ± 4 mmHg, p = 0.035), a less pronounced rise in lactate and inflammatory cytokine levels, and attenuated cardiac damage. Inhalation of NO at 20 ppm improved neurological outcomes in rats 2 to 7 days after CA and CPR. This translated into increases in 7 day survival (Control: 4; 20 ppm: 10; 40 ppm 6, (p ≤ 0.05 20 ppm vs Control and 40 ppm).ConclusionsOur study revealed that breathing NO during CPR markedly improved resuscitation success, 7-day neurological outcomes and survival in a rat model of VF-induced cardiac arrest and CPR. These results support the beneficial effects of NO inhalation after cardiac arrest and CPR.
Highlights
Inhaled nitric oxide improves outcomes when given post systemic ischemia/reperfusion injury. iNO given during cardiopulmonary resuscitation (CPR) may improve return of spontaneous circulation (ROSC) rates and functional outcome after cardiac arrest (CA)
Application of 20 ppm iNO significantly increased diastolic arterial pressure (DAP) during CPR (Fig. 1) and significantly decreased time to ROSC in comparison to untreated controls (20 ppm: 792 ± 5 s vs. 40 ppm: 798 ± 9 s vs. control: 842 ± 21 s; p = 0.02 20 ppm vs. control). This translated into pronounced increases in ROSC rates and significant differences in the 7-day survival in comparison to animals receiving no iNO treatment (Fig. 2)
While both iNO-treated groups presented with higher mean arterial pressure (MAP), lower lactate levels and concurrently higher base excess post ROSC, we only observed a statistically
Summary
Inhaled nitric oxide (iNO) improves outcomes when given post systemic ischemia/reperfusion injury. iNO given during cardiopulmonary resuscitation (CPR) may improve return of spontaneous circulation (ROSC) rates and functional outcome after cardiac arrest (CA). Inhaled nitric oxide (iNO) improves outcomes when given post systemic ischemia/reperfusion injury. INO given during cardiopulmonary resuscitation (CPR) may improve return of spontaneous circulation (ROSC) rates and functional outcome after cardiac arrest (CA). Despite improvements in pre-hospital care and the introduction of mild therapeutic hypothermia (MTH) [2], mortality rates of out-of-hospital CA victims are still high, regional variations are often reported [3, 4]. Survivors frequently suffer from moderate to severe cognitive deficits 3 months post resuscitation [5, 6]. No pharmacological agent is available to further improve outcomes for CA victims
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