Fontana J, Yard B, Stamellou E, Wenz H, Benck U, Schnuelle P, Hoeger S
Fifth Medical Department, University Medical Center Mannheim, Medical Faculty Mannheim, Ruprecht Karls University Heidelberg, Mannheim, Germany.
Fifth Medical Department, University Medical Center Mannheim, Medical Faculty Mannheim, Ruprecht Karls University Heidelberg, Mannheim, Germany.
Transplant Proc. 2014 Dec;46(10):3319-25. doi: 10.1016/j.transproceed.2014.04.020.
Brain death (BD) and cold preservation are major risk factors for an unfavorable transplantation outcome. Although donor dopamine treatment in brain-dead rats improves renal function and histology in allogeneic recipients, it remains to be assessed if this also holds true for the combinations of BD and prolonged static cold preservation.
BD was induced in F344 donor rats, which were subsequently treated with NaCl 1 mL/h (BD, n = 11), NaCl/hydroxy ethyl starch (BD-norm, n = 10), or 10 μg/min/kg dopamine (BD-dopa, n = 10). Renal grafts were harvested 4 h after BD and transplanted into bilateral nephrectomized Lewis recipients 6 h after cold preservation in University of Wisconsin solution. Renal function was evaluated by use of serum creatinine and urea concentrations at days 0, 1, 3, 5, and 10. Ten days after transplantation, recipients were killed and the renal allografts were processed for light microscopy and immune histology.
Serum urea concentrations at days 5 and 10 were significantly lower in recipients that received a renal graft from dopamine-treated rats; for serum creatinine, only a trend was observed at day 10. Immune histology revealed a lower degree of ED1-positive cells in the donor dopamine-treated group. Under light microscopy, Banff classification revealed significantly less intimal arteritis in these grafts (P < .05).
Although donor dopamine treatment clearly improves renal histology in this model, the beneficial effect on early renal function was marginal. It remains to be assessed if donor dopamine treatment has a beneficial effect on renal function in long-term follow-up.
脑死亡（BD）和冷藏保存是移植结果不佳的主要风险因素。虽然对脑死亡大鼠进行供体多巴胺治疗可改善同种异体受体的肾功能和组织学，但对于BD与延长静态冷藏保存相结合的情况是否也如此仍有待评估。
诱导F344供体大鼠发生BD，随后分别用1 mL/h的氯化钠溶液（BD组，n = 11）、氯化钠/羟乙基淀粉溶液（BD-正常组，n = 10）或10 μg/min/kg多巴胺（BD-多巴胺组，n = 10）进行治疗。BD发生4小时后采集肾移植器官，并在威斯康星大学溶液中冷藏保存6小时后移植到双侧肾切除的Lewis受体中。在第0、1、3、5和10天通过血清肌酐和尿素浓度评估肾功能。移植后10天，处死受体并对肾移植器官进行光镜检查和免疫组织学检查。
接受多巴胺治疗大鼠的肾移植受体在第5天和第10天的血清尿素浓度显著较低；对于血清肌酐，仅在第10天观察到一种趋势。免疫组织学显示供体多巴胺治疗组中ED1阳性细胞的程度较低。在光镜下，Banff分类显示这些移植器官中的内膜动脉炎明显较少（P < 0.05）。
虽然在该模型中供体多巴胺治疗明显改善了肾组织学，但对早期肾功能的有益作用微乎其微。供体多巴胺治疗在长期随访中对肾功能是否有有益作用仍有待评估。
