Li Ji, Yuan Tong, Zhao Xin, Lv Guo-Yue, Liu Huan-Qiu
Department of Anesthesiology, The First Hospital of Jilin University, Changchun, China.
Department of Pediatric Respiration, The First Hospital of Jilin University, Changchun, China.
Int J Immunopathol Pharmacol. 2016 Jun;29(2):300-7. doi: 10.1177/0394632016638346. Epub 2016 Mar 10.
The endothelial glycocalyx plays a critical role in the regulation of vascular structure and functions. Previous studies have demonstrated that sevoflurane, a volatile anesthetic, can preserve the endothelial glycocalyx in heart tissues against ischemia-reperfusion injury. However, little is known about the effects of sevoflurane pretreatment on the vascular structure and functions of liver tissues following ischemia-reperfusion injury. To this end, female Sprague-Dawley rats (n = 28) were anesthetized either with ketamine (80-120 mg/kg, i.p.) or with one minimum alveolar concentration (MAC) sevoflurane (2% v/v). Following in vivo hepatic ischemia procedure, the liver was isolated and reperfusion was produced. During the period of reperfusion, liver reperfusion samples were collected, and the concentrations of heparan sulfate and syndecan-1 (Syn-1), and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes, were measured. The morphology of hepatocytes and endothelial glycocalyx were then assessed by using the light and electron microscopies, respectively. Ischemia-reperfusion increased the release of HS and Syn-1, and elevated the levels of ALT and AST in a time-dependent manner. However, sevoflurane pretreatment reduced the release of HS and Syn-1and attenuated the levels of ALT and AST, in a time-dependent manner, as compared with ketamine pretreatment. Furthermore, sevoflurane pretreatment decreased the shedding of endothelial glycocalyx and hepatocytes necrosis. Sevoflurane pretreatment preserved the endothelial glycocalyx in the liver tissue against ischemia-reperfusion injury. The effect appears to help protect hepatocytes against ischemia-reperfusion-induced necrosis.
内皮糖萼在血管结构和功能的调节中起关键作用。先前的研究表明，挥发性麻醉剂七氟醚可保护心脏组织中的内皮糖萼免受缺血再灌注损伤。然而，关于七氟醚预处理对缺血再灌注损伤后肝脏组织血管结构和功能的影响知之甚少。为此，将28只雌性Sprague-Dawley大鼠用氯胺酮（80-120mg/kg，腹腔注射）或1个最低肺泡浓度（MAC）的七氟醚（2% v/v）麻醉。在进行体内肝脏缺血操作后，分离肝脏并进行再灌注。在再灌注期间，收集肝脏再灌注样本，测量硫酸乙酰肝素和多配体蛋白聚糖-1（Syn-1）的浓度以及天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）的水平。然后分别通过光学显微镜和电子显微镜评估肝细胞和内皮糖萼的形态。缺血再灌注以时间依赖性方式增加了HS和Syn-1的释放，并升高了ALT和AST的水平。然而，与氯胺酮预处理相比，七氟醚预处理以时间依赖性方式减少了HS和Syn-1的释放，并减弱了ALT和AST的水平。此外，七氟醚预处理减少了内皮糖萼的脱落和肝细胞坏死。七氟醚预处理可保护肝脏组织中的内皮糖萼免受缺血再灌注损伤。这种作用似乎有助于保护肝细胞免受缺血再灌注诱导的坏死。
