Department of Anaesthesiology and Intensive Care Medicine, Schleswig-Holstein University Hospital, Campus Kiel, Schwanenweg 21, D-24105 Kiel, Germany.
Crit Care. 2011;15(5):R241. doi: 10.1186/cc10496. Epub 2011 Oct 19.
In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation.
Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours. Neurological function was assessed 24 hours after return of spontaneous circulation. The effects on myocardial and cerebral damage, especially on inflammation, apoptosis and tissue remodeling, were studied using cellular and molecular approaches.
Animals treated with SEVO had lower peak troponin T levels (median [IQR]) (CONTROL vs SEVO = 0.31 pg/mL [0.2 to 0.65] vs 0.14 pg/mL [0.09 to 0.25]; P < 0.05) and improved left ventricular systolic and diastolic function compared to the CONTROL group (P < 0.05). SEVO was associated with a reduction in myocardial IL-1β protein concentrations (0.16 pg/μg total protein [0.14 to 0.17] vs 0.12 pg/μg total protein [0.11 to 0.14]; P < 0.01), a reduction in apoptosis (increased procaspase-3 protein levels (0.94 arbitrary units [0.86 to 1.04] vs 1.18 arbitrary units [1.03 to 1.28]; P < 0.05), increased hypoxia-inducible factor (HIF)-1α protein expression (P < 0.05) and increased activity of matrix metalloproteinase 9 (P < 0.05). SEVO did not, however, affect neurological deficit score or cerebral cellular and molecular pathways.
SEVO reduced myocardial damage and dysfunction after cardiopulmonary resuscitation in the early postresuscitation period. The reduction was associated with a reduced rate of myocardial proinflammatory cytokine expression, apoptosis, increased HIF-1α expression and increased activity of matrix metalloproteinase 9. Early administration of SEVO may not, however, improve neurological recovery.
本研究旨在探讨七氟醚（SEVO）在心肺复苏后的药物性后处理中对猪模型的神经和心脏保护作用。
22 头猪进行心脏骤停。室颤 8 分钟和基础生命支持 2 分钟后，开始进行高级心脏生命支持。自主循环恢复成功后（N=16），动物随机分为（1）异丙酚（CONTROL）麻醉或（2）SEVO 麻醉 4 小时。自主循环恢复后 24 小时评估神经功能。使用细胞和分子方法研究心肌和脑损伤的影响，特别是炎症、细胞凋亡和组织重塑的影响。
与 CONTROL 组相比，接受 SEVO 治疗的动物的肌钙蛋白 T 峰值水平（中位数[IQR]）更低（CONTROL 组 vs SEVO 组=0.31pg/ml[0.2 至 0.65]vs0.14pg/ml[0.09 至 0.25]；P<0.05），左心室收缩和舒张功能改善（P<0.05）。SEVO 与心肌 IL-1β 蛋白浓度降低相关（0.16pg/μg 总蛋白[0.14 至 0.17] vs 0.12pg/μg 总蛋白[0.11 至 0.14]；P<0.01），细胞凋亡减少（促半胱氨酸天冬氨酸蛋白酶-3 蛋白水平增加（0.94 任意单位[0.86 至 1.04] vs 1.18 任意单位[1.03 至 1.28]；P<0.05），缺氧诱导因子（HIF）-1α 蛋白表达增加（P<0.05），基质金属蛋白酶 9 活性增加（P<0.05）。然而，SEVO 并没有影响神经缺陷评分或脑细胞和分子途径。
SEVO 减少心肺复苏后早期再灌注期的心肌损伤和功能障碍。减少与心肌前炎症细胞因子表达减少、细胞凋亡减少、HIF-1α 表达增加和基质金属蛋白酶 9 活性增加有关。然而，早期给予 SEVO 可能不会改善神经恢复。
Zotero 插件
