Wilhelm M J, Pratschke J, Beato F, Taal M, Kusaka M, Hancock W W, Tilney N L
Surgical Research Laboratory, Harvard Medical School and the Department of Surgery, Brigham and Women's Hospital, Cambridge, Massachusetts, USA.
Circulation. 2000 Nov 7;102(19):2426-33. doi: 10.1161/01.cir.102.19.2426.
Donor brain death upregulates expression of inflammatory mediators in the heart. It is hypothesized that these nonspecific changes trigger and amplify acute rejection in unmodified recipients compared with hearts from normal living donors. We examined the inflammatory and immunological consequences of gradual-onset donor brain death on cardiac allografts after transplantation.
Functioning hearts were engrafted from normotensive donors after 6 hours of ventilatory support. Hearts from brain-dead rats (Fisher, F344) were rejected significantly earlier (mean+/-SD, 9. 3+/-0.6 days) by their (Lewis) recipients than hearts from living donor controls (11.6+/-0.7 days, P=0.03). The inflammatory response of such organs was accelerated, with rapid expression of cytokines, chemokines, and adhesion molecules and brisk infiltration of associated leukocyte populations. Upregulation of major histocompatibility class II antigens increased organ immunogenicity. Acute rejection evolved in hearts from brain-dead donors more intensely and at a significantly faster rate than in controls.
Donor brain death is deleterious to transplanted hearts. The resultant upregulation of inflammatory factors provokes host immune mechanisms and accelerates the acute rejection process in unmodified hosts.
供体脑死亡会上调心脏中炎症介质的表达。据推测，与来自正常活体供体的心脏相比，这些非特异性变化会引发并放大未处理受体中的急性排斥反应。我们研究了移植后供体脑死亡逐渐发生对心脏同种异体移植的炎症和免疫影响。
在通气支持6小时后，将功能正常的心脏移植自血压正常的供体。脑死亡大鼠（Fisher，F344）的心脏被其（Lewis）受体排斥的时间明显早于活体供体对照组（平均±标准差，9.3±0.6天对11.6±0.7天，P = 0.03）。此类器官的炎症反应加速，细胞因子、趋化因子和黏附分子迅速表达，相关白细胞群体大量浸润。主要组织相容性复合体II类抗原的上调增加了器官的免疫原性。脑死亡供体心脏的急性排斥反应比对照组更强烈且进展明显更快。
供体脑死亡对移植心脏有害。由此导致的炎症因子上调会激发宿主免疫机制，并加速未处理宿主中的急性排斥反应过程。
