Abstract：
Sudden cardiac arrest (CA) is the third leading cause of death. Immediate reoxygenation with high concentrations of supplemental oxygen (O2) during cardiopulmonary resuscitation (CPR) is recommended according to the current guidelines for adult CA. However, a point in controversy exists because of the known harm of prolonged exposure to 100% O2. Therefore, there have been much debate on an optimal use of supplemental O2, yet little is known about the duration and dosage of O2 administration. To test whether supplying a high concentration of O2 during CPR and post resuscitation is beneficial or harmful, rats subjected to 10-minute asphyxia CA were administered either 100% O2 (n = 8) or 30% O2 (n = 8) for 2 hours after CPR. Two hours after initiating CPR, the brain, lung, and heart tissues were collected to compare mRNA gene expression levels of inflammatory cytokines, apoptotic and oxidative stress-related markers. The 100% O2 group had significantly shorter time to return of spontaneous circulation (ROSC) than the 30% O2 group (62.9 ± 2.2 and 77.5 ± 5.9 seconds, respectively, P < 0.05). Arterial blood gas analysis revealed that the 100% O2 group had significantly higher PaCO2 (49.4 ± 4.9 mmHg and 43.0 ± 3.0 mmHg, P < 0.01), TCO2 (29.8 ± 2.7 and 26.6 ± 1.1 mmol/L, P < 0.05), HCO3- (28.1 ± 2.4 and 25.4 ± 1.2 mmol/L, P < 0.05), and BE (2.6 ± 2.3 and 0.1 ± 1.4 mmol/L, P < 0.05) at 2 hours after initiating CPR, but no changes in pH (7.37 ± 0.03 and 7.38 ± 0.03, ns). Inflammation- (Il6, Tnf) and apoptosis- (Casp3) related mRNA gene expression levels were significantly low in the 100% O2 group in the brain, however, oxidative stress moderator Hmox1 increased in the 100% O2 group. Likewise, mRNA gene expression of Icam1, Casp9, Bcl2, and Bax were low in the 100% O2 group in the lung. Contrarily, mRNA gene expression of Il1b and Icam1 were low in the 30% O2 group in the heart. Supplying 30% O2 during and after CPR significantly delayed the time to ROSC and increased inflammation-/apoptosis- related gene expression in the brain and lung, indicating that insufficient O2 was associated with unfavorable biological responses post CA, while prolonged exposure to high-concentration O2 should be still cautious in general.
摘要：
心脏骤停（CA）是第三大死亡原因。根据目前的成人CA指南，建议在心肺复苏（CPR）期间使用高浓度的补充氧气（O2）立即复氧。然而,由于已知长期暴露于100％O2的危害，因此存在争议。因此,关于补充O2的最佳使用一直存在很多争论，但对O2给药的持续时间和剂量知之甚少。为了测试在心肺复苏和复苏后供应高浓度氧气是有益还是有害，接受10分钟窒息CA的大鼠在CPR后给予100%O2(n=8)或30%O2(n=8)2小时。开始心肺复苏后两小时，大脑,肺，收集和心脏组织，比较炎性细胞因子的mRNA基因表达水平，凋亡和氧化应激相关标志物。100％O2组恢复自主循环（ROSC）的时间明显短于30％O2组（62.9±2.2和77.5±5.9秒，分别,P<0.05)。动脉血气分析显示，100％O2组的PaCO2明显高于（49.4±4.9mmHg和43.0±3.0mmHg，P<0.01),TCO2（29.8±2.7和26.6±1.1mmol/L，P<0.05),HCO3-（28.1±2.4和25.4±1.2mmol/L，P<0.05),和BE（2.6±2.3和0.1±1.4mmol/L，P<0.05)在开始心肺复苏后2小时，但pH值无变化（7.37±0.03和7.38±0.03，ns）。100%O2组脑内炎症-(Il6,Tnf)和凋亡-(Casp3)相关mRNA表达水平显著较低,然而,氧化应激调节剂Hmox1在100％O2组中增加。同样，Icam1、Casp9、Bcl2和Bax的mRNA基因表达在肺组织中100%O2组较低。相反，Il1b和Icam1的mRNA基因表达在心脏中30%O2组较低。在CPR期间和之后供应30%O2显著延迟了ROSC的时间,并增加了脑和肺中炎症/凋亡相关基因的表达,表明O2不足与CA后不利的生物反应有关，而长期暴露于高浓度O2一般仍应谨慎。
