Brief inhalation of nitric oxide increases resuscitation success and improves 7-day-survival after cardiac arrest in rats: a randomized controlled animal study.
Brief inhalation of nitric oxide increases resuscitation success and improves 7-day-survival after cardiac arrest in rats: a randomized controlled animal study.
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DOI：
10.1186/s13054-015-1128-x
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发表时间：
2015-11-17
期刊：
影响因子：
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通讯作者：
Fries M
中科院分区：
文献类型：
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作者：
Brücken A;Derwall M;Bleilevens C;Stoppe C;Götzenich A;Gaisa NT;Weis J;Nolte KW;Rossaint R;Ichinose F;Fries M
吸入一氧化氮（iNO）可改善全身缺血/再灌注损伤后的预后。因此，在心肺复苏（CPR）期间给予iNO可能改善心脏骤停（CA）后的自发循环恢复（ROSC）率和功能结局。30只雄性Sprague-Dawley大鼠进行10分钟的CA和至少3分钟的CPR。动物在心肺复苏术期间随机接受0 （n = 10，对照）、20 （n = 10, 20 ppm）或40 (n = 10, 40 ppm) ppm iNO，直至ROSC后30分钟。在实验后的7天里，每天评估神经功能缺损评分。第7天，取脑组织、心脏和血液进行组织学和生化评价。在心肺复苏术中，20 ppm iNO显著增加舒张动脉压（对照组：57±5.04 mmHg; 20 ppm: 71.57±57.3 mmHg, p < 0.046），缩短至ROSC的时间（对照组：842±21 s； 20 ppm: 792±5 s, p = 0.02）。ROSC后30分钟，20ppm iNO导致平均动脉压升高（对照组：83±4 mmHg； 20ppm: 98±4 mmHg, p = 0.035），乳酸和炎症细胞因子水平升高不太明显，心脏损伤减轻。在CA和CPR后2至7天，吸入20 ppm的NO可改善大鼠的神经预后。这转化为7天生存率的增加(对照组：4；20 ppm: 10; 40 ppm 6, （p≤0.05 20 ppm与对照组和40 ppm）。我们的研究表明，在心肺复苏术中呼吸NO可显著提高vf诱导的心脏骤停和心肺复苏术大鼠模型的复苏成功率、7天神经预后和生存率。这些结果支持心脏骤停和心肺复苏术后吸入NO的有益作用。
Inhaled 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). Thirty 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. During 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). Our 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.