ROLE OF PLATELETS IN HEPATIC ALLOGRAFT PRESERVATION INJURY IN THE RAT
ROLE OF PLATELETS IN HEPATIC ALLOGRAFT PRESERVATION INJURY IN THE RAT
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DOI：
10.1002/hep.1840180324
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发表时间：
1993-09-01
期刊：
影响因子：
13.5
通讯作者：
STRASBERG, SM
中科院分区：
文献类型：
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作者：
CYWES, R;PACKHAM, MA;STRASBERG, SM
冷保存对肝窦衬里细胞的损伤。这种损伤在再灌注时加重，部分原因是白细胞的粘附。血小板还粘附于活化的内皮表面。在这项研究中，我们研究了血小板在保存损伤中的作用。我们的具体目标是确定保存大鼠肝脏再灌注时血小板粘附的程度是否与冷缺血或热缺血的持续时间有关，以及血小板粘附是否导致同种异体移植物损伤。我们还研究了血小板活化对粘附和损伤的影响。将大鼠肝脏在威斯康星州大学溶液中于1 ℃保存不同的时间，然后用加入未活化的分离大鼠血小板的Krebs-Henseleit溶液在分离的灌注大鼠肝脏系统上再灌注3小时。其他肝脏在再灌注前复温或用活化血小板再灌注。在所有研究中，血小板均从循环中丢失;循环血小板的减少百分比取决于保存时间的长短。初始血小板浓度不影响回路中血小板的减少率。再灌注前复温可增加血小板粘附性，预先激活也可增加粘附性。用电子显微镜我们确定，血小板粘附在内皮细胞或内皮细胞残余物的小聚集体。粘附血小板出现更多的激活，并含有较少的颗粒比未灌注血小板。通过释放转氨酶到灌注液中来测量肝损伤，通过较长时间的冷保存和在方案中添加复温来恶化。在这种情况下，血小板的存在会加剧伤害。血小板的预先活化也增加了损伤的程度。这些研究表明血小板在冷缺血再灌注损伤中具有重要作用。
Cold preservation of liver allografts injures hepatic sinusoidal lining cells. This injury is exacerbated on reperfusion, in part because of adhesion of leukocytes. Platelets also adhere to activated endothelial surfaces. In this study we examined the role of platelets in preservation injury. Our specific aim was to determine whether the degree of platelet adhesion on reperfusion of preserved rat livers was related to duration of cold or warm ischemia and whether platelet adhesion resulted in injury to allografts. We also examined the effect of prior activation of platelets on adhesion and injury. Rat livers were preserved at 1-degrees-C for different time periods in University of Wisconsin solution and then reperfused for 3 hr on the isolated perfused rat liver system with Krebs-Henseleit solution to which unactivated isolated rat platelets were added. Other livers were rewarmed before reperfusion or reperfused with activated platelets. Platelets were lost from the circulation in all studies; the percentage reduction of circulating platelets was dependent on the length of preservation. The initial platelet concentration did not affect the rate of reduction of platelets in the circuit. Rewarming before reperfusion increased platelet adherence, and prior activation also increased adherence. With electron microscopy we determined that platelets adhered in small aggregates to endothelial cells or endothelial cell remnants. Adherent platelets appeared more activated and contained fewer granules than did unperfused platelets. Liver injury as measured by release of transaminases into perfusate was worsened by longer periods of cold preservation and by addition of rewarming to the protocol. The presence of platelets under these circumstances aggravated injury. Prior activation of platelets also increased the extent of injury. These studies show that platelets have an important role in cold preservation-reperfusion injury.