Choi Eun Kyung, Baek Jongyoon, Park Sangyoung, Baek Suk Hwan, Choi Joon-Hyuk, Lee Chae Hoon, Sung Eon-Gi, Jee Daelim
Department of Anesthesiology and Pain Medicine, Yeungnam University College of Medicine, Daegu, Korea.
Department of Biochemistry and Molecular Biology, Yeungnam University College of Medicine, Daegu, Korea.
J Surg Res. 2018 Feb;222:26-33. doi: 10.1016/j.jss.2017.09.017. Epub 2017 Oct 28.
Hepatic innate immune cells are considered to play a central role in the early phase of hepatic ischemia reperfusion (IR) injury. Transfusion of old red blood cells (RBCs) is known to prime immune cells, and transfusion before IR may exacerbate liver injury because of the expected hyperresponsiveness of immune cells.
Twenty-four Sprague-Dawley rats were divided into four groups: sham operation (Sham); hepatic IR only (IR Control); and two transfusion groups, preischemic (Pre-T) and postischemic (Post-T), in which allogeneic RBCs stored for 2 weeks were transfused before hepatic IR or after reperfusion, respectively. Partial hepatic ischemia was induced for 90 min, and reperfusion was allowed for 120 min. Serum alanine transaminase levels, area of necrosis, and apoptotic cells were then assessed. Inflammatory (tumor necrosis factor alpha, interleukin 1 beta [IL-1β], IL-6, IL-10, and cyclooxygenase 2) and oxidative mediators (heme oxygenase 1, superoxide dismutase, and glutathione peroxidase 1) were assessed for elucidating the relevant mechanisms underlying the hepatic injury.
Pre-T, but not Post-T, showed increased serum alanine transaminase levels than IR Control (P < 0.05). Area of necrosis was more severe in Pre-T than in IR Control or Post-T (P < 0.01), and apoptotic cells were also more abundant in Pre-T than in IR Control (P < 0.01). tumor necrosis factor alpha and IL-6 levels were higher in Pre-T than in IR Control or Post-T (P < 0.05), with no significant difference in cytoprotective protein levels.
Preischemic transfusion of old RBCs aggravated hepatic injury. Inflammatory cytokines seemed to play a crucial role in liver injury exacerbation. Our results indicate that transfusion before hepatic ischemia may be detrimental.
肝脏固有免疫细胞被认为在肝脏缺血再灌注（IR）损伤的早期阶段起核心作用。已知输注衰老红细胞（RBC）会使免疫细胞致敏，并且在IR之前进行输血可能会因免疫细胞预期的高反应性而加重肝损伤。
将24只Sprague-Dawley大鼠分为四组：假手术组（Sham）；仅肝脏IR组（IR对照组）；以及两个输血组，即缺血前（Pre-T）组和缺血后（Post-T）组，其中分别在肝脏IR之前或再灌注后输注储存2周的异体RBC。诱导部分肝脏缺血90分钟，然后进行120分钟的再灌注。随后评估血清丙氨酸转氨酶水平、坏死面积和凋亡细胞。评估炎症介质（肿瘤坏死因子α、白细胞介素1β[IL-1β]、IL-6、IL-10和环氧化酶2）和氧化介质（血红素加氧酶1、超氧化物歧化酶和谷胱甘肽过氧化物酶1）以阐明肝损伤的相关潜在机制。
Pre-T组而非Post-T组的血清丙氨酸转氨酶水平高于IR对照组（P<0.05）。Pre-T组的坏死面积比IR对照组或Post-T组更严重（P<？0.01），并且Pre-T组的凋亡细胞也比IR对照组更丰富（P<0.01）。Pre-T组的肿瘤坏死因子α和IL-6水平高于IR对照组或Post-T组（P<0.05），细胞保护蛋白水平无显著差异。
缺血前输注衰老RBC会加重肝损伤。炎症细胞因子似乎在肝损伤加重中起关键作用。我们的结果表明，肝脏缺血前输血可能有害。
