Li Yong, Wang Zehua, Hu Qiangfu, Yu Dapeng, Gao Ju, Yang Liuqing, Ge Yali, Chen Ping, Zong Liang
Department of Anesthesiology, Su Bei People's Hospital of Jiangsu Province, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Department of Anesthesiology, Heji Hospital, Changzhi University, Changzhi Medical College, Changzhi, Shanxi 046000, P.R. China.
Biomed Rep. 2017 Oct;7(4):361-364. doi: 10.3892/br.2017.976. Epub 2017 Sep 5.
Myocardial ischemia/reperfusion (I/R) injury is usually caused by resuscitation following cardiac arrest. The aim of the present study was to investigate the influence of sevoflurane postconditioning on the myocardial ultrastructure induced by cardiac arrest and successful resuscitation in mature rabbits. A total of 32 rabbits were randomly and equally divided into an I/R group (I/R group), a hypothermia group (H group), a sevoflurane postconditioning group (S group), and hypothermia plus sevoflurane postconditioning group (H + S group). Interleukin (IL)-8 and IL-10 levels in blood were evaluated at four different time points (1 h pre-ischemia: T1; 1, 2 and 3 h after reperfusion: T2, T3 and T4, respectively). The myocardial ultrastructure was evaluated by microscope after the rabbits were scarified. Plasma levels of IL-8 and IL-10 increased in all of the groups from T2. However, compared with the I/R group from T3 and T4, downregulation of IL-8 was significant in the S and H + S groups (P<0.05), and the result of intra-group comparison demonstrated that the level of serum IL-8 was the lowest in the H + S group (P<0.05). By contrast, upregulation of IL-10 was significantly higher in the S and H + S groups (P<0.05), particularly in the H + S group. Notably, ultrastructure damage of the myocardium was significantly lighter, and the structural integrity of the myocardium in the H + S group was better when compared with that of the S group. Thus, sevoflurane postconditioning plus hypothermia protected the myocardial ultrastructure following cardiopulmonary resuscitation by suppressing inflammatory effects.
心肌缺血/再灌注（I/R）损伤通常由心脏骤停后的复苏引起。本研究旨在探讨七氟醚后处理对成年兔心脏骤停及成功复苏后心肌超微结构的影响。将32只兔随机均分为缺血/再灌注组（I/R组）、低温组（H组）、七氟醚后处理组（S组）和低温加七氟醚后处理组（H + S组）。在四个不同时间点（缺血前1小时：T1；再灌注后1、2和3小时：分别为T2、T3和T4）评估血液中白细胞介素（IL）-8和IL-10水平。兔处死后通过显微镜评估心肌超微结构。所有组从T2开始血浆中IL-8和IL-10水平均升高。然而，与I/R组在T3和T4时相比，S组和H + S组中IL-8下调显著（P<0.05），组内比较结果显示H + S组血清IL-8水平最低（P<0.05）。相比之下，S组和H + S组中IL-10上调显著更高（P<0.05），尤其是在H + S组。值得注意的是，与S组相比，H + S组心肌超微结构损伤明显更轻，心肌结构完整性更好。因此，七氟醚后处理加低温通过抑制炎症作用保护了心肺复苏后的心肌超微结构。
