Knöferl M W, Angele M K, Ayala A, Cioffi W G, Bland K I, Chaudry I H
Center for Surgical Research and Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence 02903, USA.
J Trauma. 1999 Jan;46(1):23-33. doi: 10.1097/00005373-199901000-00005.
Although rapid fluid resuscitation continues to be an important component of the initial therapy for trauma patients, it remains unknown whether the rate of fluid administration after trauma-hemorrhage has any deleterious or beneficial effects on immunity.
Male C3H/HeN mice were subjected to sham operation or soft-tissue trauma (midline laparotomy) and hemorrhagic shock (mean arterial blood pressure of 35+/-5 mm Hg for 90 minutes) followed by resuscitation with four times the volume of shed blood in the form of lactated Ringer's solution over 30 minutes (rapid rate), 60 minutes (moderate rate), or 120 minutes (slow rate). The animals were killed at either 4 hours or 4 days after the end of trauma-hemorrhage. Spleens were harvested and splenocyte interleukin (IL)-3 and interferon-gamma (IFN-gamma) release as well as splenic macrophage IL-1beta and IL-6 release were determined.
The results indicate that at 4 hours after trauma-hemorrhage, splenocyte IL-3 and IFN-gamma release were significantly depressed in all animals subjected to trauma-hemorrhage compared with sham-operated animals. At 4 days after trauma-hemorrhage, splenocyte IL-3 and IFN-gamma release were restored in mice resuscitated with the slow rate of resuscitation; however, the release of these cytokines remained significantly depressed in animals resuscitated with the moderate or rapid rates. Splenic macrophage IL-1beta and IL-6 release were significantly depressed at 4 hours after trauma-hemorrhage. At 4 days after trauma-hemorrhage, the release of these proinflammatory cytokines was still depressed in animals resuscitated with the rapid rate. In contrast, splenic macrophage IL-1beta and IL-6 release were restored in mice receiving the slow rate of resuscitation.
These results suggest that a slower rate of fluid resuscitation after trauma-hemorrhage leads to a faster restoration of the depressed cell-mediated immunity, whereas rapid fluid resuscitation produces a prolonged depression of immune responses. In view of this, we propose that a prospective clinical study of this type must be performed in a select group of trauma patients to determine whether or not a slower rate of fluid resuscitation also improves immune responses in trauma patients.
尽管快速液体复苏仍然是创伤患者初始治疗的重要组成部分，但创伤出血后液体输注速率对免疫是否有任何有害或有益影响仍不清楚。
雄性C3H/HeN小鼠接受假手术或软组织创伤（中线剖腹术）和失血性休克（平均动脉血压为35±5毫米汞柱，持续90分钟），随后在30分钟内（快速输注速率）、60分钟内（中等输注速率）或120分钟内（缓慢输注速率）以失血量四倍的乳酸林格氏液形式进行复苏。在创伤出血结束后4小时或4天处死动物。采集脾脏并测定脾细胞白细胞介素（IL）-3和干扰素-γ（IFN-γ）释放以及脾巨噬细胞IL-1β和IL-6释放。
结果表明，与假手术动物相比，创伤出血后4小时，所有经历创伤出血的动物脾细胞IL-3和IFN-γ释放均显著降低。创伤出血后4天，缓慢复苏速率的小鼠脾细胞IL-3和IFN-γ释放恢复；然而，中等或快速复苏速率的动物中这些细胞因子的释放仍显著降低。创伤出血后4小时，脾巨噬细胞IL-1β和IL-6释放显著降低。创伤出血后4天，快速复苏速率的动物中这些促炎细胞因子的释放仍降低。相比之下，接受缓慢复苏速率的小鼠脾巨噬细胞IL-1β和IL-6释放恢复。
这些结果表明，创伤出血后较慢的液体复苏速率导致细胞介导免疫抑制的更快恢复，而快速液体复苏导致免疫反应的长期抑制。鉴于此，我们建议必须在一组特定的创伤患者中进行此类前瞻性临床研究，以确定较慢的液体复苏速率是否也能改善创伤患者的免疫反应。
