Surgery Research Laboratory, Department of Surgery, University Medical Center Groningen, University of Groningen, The Netherlands.
Crit Care Med. 2010 Apr;38(4):1155-61. doi: 10.1097/CCM.0b013e3181cf6e78.
We hypothesized that donor treatment of deceased brain dead donors would lead to a decrease in inflammatory responses seen in brain death and lead to a restoration of kidney function.
A standardized slow-induction rat brain death model followed by evaluation of kidney function in an isolated perfused kidney model.
Surgery Research Laboratory, University Medical Center Groningen, the Netherlands.
Male Fisher rats.
Donor treatment with erythropoietin, carbamylated erythropoietin, which lacks erythropoietic activity, or vehicle.
In brain death, carbamylated erythropoietin and, to a lesser extent, erythropoietin were able to decrease the expression of several proinflammatory genes and to decrease the infiltration of polymorphonuclear cells in the kidney. No effect on tubular injury parameters was seen. Kidney function decreased almost by 50% after brain death but was fully restored after treatment with both carbamylated erythropoietin and erythropoietin.
Carbamylated erythropoietin can inhibit the inflammatory response caused by brain death more effectively than erythropoietin, whereas both substances can restore kidney function after brain death.
我们假设对脑死亡供体进行供体治疗，将降低脑死亡中观察到的炎症反应，并恢复肾功能。
标准化的慢诱导大鼠脑死亡模型，随后在离体灌注肾模型中评估肾功能。
荷兰格罗宁根大学医学中心外科研究实验室。
雄性 Fisher 大鼠。
给予促红细胞生成素、无促红细胞生成活性的氨甲酰化促红细胞生成素或载体治疗供体。
在脑死亡中，氨甲酰化促红细胞生成素和促红细胞生成素可降低几种促炎基因的表达，并减少多形核细胞在肾脏中的浸润。但对肾小管损伤参数没有影响。脑死亡后，肾功能几乎下降了 50%，但在用氨甲酰化促红细胞生成素和促红细胞生成素治疗后完全恢复。
氨甲酰化促红细胞生成素抑制脑死亡引起的炎症反应的效果优于促红细胞生成素，而这两种物质都可以恢复脑死亡后的肾功能。
