标题：Propofol attenuates myocardial ischemia reperfusion injury partly through inhibition of resident cardiac mast cell activation
作者：Yu, Xiaoqian; Sun, Xiaotong; Zhao, Meng; Hou, Yonghao; Li, Jingxin; Yu, Jingui; Hou, Yuedong
作者机构：[Yu, Xiaoqian; Sun, Xiaotong; Zhao, Meng; Hou, Yonghao; Yu, Jingui; Hou, Yuedong] Shandong Univ, Dept Anesthesiol, Qilu Hosp, 107 Wen Hua Xi Rd, Jinan 更多
通讯作者：Yu, JG;Hou, YD
通讯作者地址：[Yu, JG; Hou, YD]Shandong Univ, Dept Anesthesiol, Qilu Hosp, 107 Wen Hua Xi Rd, Jinan 250012, Shandong, Peoples R China.
关键词：Propofol; Compound48/80; Mast cell; Myocardial ischemia reperfusion; injury
摘要：Cardiac mast cell activation is involved in the process of myocardial ischemia reperfusion (I/R) injury and exacerbates myocardial infarction. Propofol, an anesthetic with antioxidant property, can reduce myocardial infarct size in I/R injury. The present study was designed to investigate whether propofol can attenuate myocardial I/R injury by inhibiting resident cardiac mast cell activation by a Langendorff model. Thirty rats were randomly assigned to 5 groups (n = 6 per group): control group and four test groups (I/R, I/R + compound 48/80, I/R + propofol, I/R + compound 48/80 + propofol). Cultured RBL-2H3 cells were pretreated with propofol and subjected to mast cell degranulator compound48/80 (C48/80).Microscopically, degradation of myofibrillar and degranulation of mast cells were studied using hematoxylin-eosin toluidine blue staining techniques. After the effluent was assayed for tryptase, LDH, CK-MB and aid, myocardial tissue was evaluated for cytokine levels and infarct area. Heart subjected to I/R showed significantly increased expression of cytokines (TNF-alpha and IL-6), LDH, CK-MB and cTnI. In addition, the I/R-induced heart also showed greater histopathological injury and a larger infarction zone, following increased mast cell degranulation with concomitant rise in tryptase. Mast cell degranulation by C48/80 further aggravated I/R injury. However, all of these effects were suppressed by propofol pretreatment, which also abrogated C48/80-mediated exacerbation of I/R injury. Also, propofol attenuated the C48/80-evoked tryptase and histamine release in RBL-2H3 cells. It is concluded that pretreatment of propofol confers protection against I/R injury partly by inhibiting resident cardiac mast cell activation.