THE HYDROCORTISONE PROTECTION OF GLYCOCALYX ON THE INTESTINAL CAPILLARY ENDOTHELIUM DURING SEVERE ACUTE PANCREATITIS
THE HYDROCORTISONE PROTECTION OF GLYCOCALYX ON THE INTESTINAL CAPILLARY ENDOTHELIUM DURING SEVERE ACUTE PANCREATITIS
复制标题
重症急性胰腺炎时糖萼的氢化可的松对肠毛细血管内皮的保护作用。
DOI：
10.1097/shk.0000000000000326
复制
发表时间：
2015-05-01
期刊：
影响因子：
3.1
通讯作者：
Liang, Ting-Bo
中科院分区：
文献类型：
--
作者：
Gao, Shun-Liang;Zhang, Yun;Liang, Ting-Bo
重症急性胰腺炎（SAP）继发的肠道微循环功能障碍可导致肠黏膜屏障损伤、肠道菌群移位和脓毒症。血管内皮上的糖萼通过多种机制有助于维持其正常功能，包括调节血管通透性和抑制细胞间黏附。目前尚不清楚胰腺炎是否通过损伤糖萼而导致肠黏膜屏障损伤，以及稳定糖萼是否可作为SAP期间维持肠黏膜屏障完整性的潜在治疗靶点。向Sprague - Dawley大鼠的胰管内注射牛磺胆酸钠诱导SAP。通过激光多普勒测速仪、电子显微镜以及肠系膜上静脉中硫酸乙酰肝素、多配体蛋白聚糖 - 1和肿瘤坏死因子 - α（TNF - α）的水平来评估肠道灌注、内皮糖萼的变化以及相关分子机制。评估了氢化可的松治疗对SAP期间肠道微循环的保护作用。大鼠SAP发病3小时后，肠道血管内皮的糖萼开始降解。到12小时时，观察到肠道灌注明显减少。肠系膜上静脉中TNF - α水平同时升高，提示TNF - α参与了糖萼的降解。使用氢化可的松后，肠道灌注得到改善，糖萼的降解减少。糖萼的降解与肠道微循环功能障碍有关。TNF - α的大量释放参与了这一过程并导致糖萼降解。氢化可的松可能是预防这一过程的良好治疗方法。
Malfunctioning of the intestinal microcirculation secondary to severe acute pancreatitis (SAP) can cause injuries to the intestinal mucosal barrier, translocation of gut flora, and sepsis. The glycocalyx on the vascular endothelium helps maintain its normal function through multiple mechanisms, including regulation of vascular permeability and inhibition of intercellular adhesion. It is unknown that whether pancreatitis inflicts injuries to the intestinal mucosal barrier through damaging glycocalyx or stabilizing glycocalyx can be a potential therapeutic target in maintaining the integrity of the intestinal mucosal barrier during SAP. Injecting sodium taurocholate into the pancreatic duct of Sprague-Dawley rats induced SAP. Intestinal perfusion, changes in endothelial glycocalyx, and the associated molecular mechanisms were assessed by laser Doppler velocimetry, electron microscopy, and the levels of heparan sulfate, syndacan-1, and tumor necrosis factor-alpha (TNF-alpha) in the superior mesenteric vein. Protective effects of hydrocortisone treatment in the intestinal microcirculation during SAP were evaluated. Degradation of the glycocalyx in intestinal vascular endothelium developed 3 h after the onset of SAP in rats. By 12 h, significant reduction of intestinal perfusion was observed. The concomitant elevated levels of TNF-alpha in the superior mesenteric vein suggest that TNF-alpha is involved in the degradation of the glycocalyx. With the use of hydrocortisone, intestinal perfusion was improved and the degradation of glycocalyx was reduced. The degradation of glycocalyx is involved in the malfunction of the intestinal microcirculation. The massive release of TNF-alpha participates in this process and leads to glycocalyx degradation. Hydrocortisone may be a good therapy to prevent this process.