Department of Emergency, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China.
Chin Med J (Engl). 2012 Jun;125(12):2163-7.
Hemorrhagic shock induces immune dysfunction. Regulatory T cells (Tregs), T-helper (Th) cells, and cytotoxic T-lymphocytes (CTLs) can execute many crucial actions in immune and inflammatory responses. This study was conducted to investigate the early pathophysiological changes of CD4(+)CD25(+)Foxp3(+) Treg and Th1/Th2, Tc1/Tc2 profiles in the peripheral blood of rats with controlled hemorrhagic shock and no fluid resuscitation.
A rat model of controlled hemorrhagic shock with no fluid resuscitation was established. Peripheral blood samples were taken before and four hours after hemorrhagic shock with no fluid resuscitation. Three color flow cytometry was used to detect Tregs, Th1, Th2, Tc1 and Tc2 cells in the samples.
In the peripheral blood of rats, the percentage of Tregs four hours after hemorrhagic shock was significantly lower than before hemorrhagic shock (P = 0.001). The ratios of Th1/Th2 and Tc1/Tc2 were changed from (23.08 ± 8.98)% to (23.91 ± 15.36)%, and from (40.40 ± 21.56)% to (65.48 ± 23.88)%, respectively.
At an early stage, the advent of hemorrhagic shock is related to an early decrease of Tregs, and a mild shift in the Th1/Th2, Tc1/Tc2 balance toward Th1 and Tc1 dominance. These changes are part of a hyper-inflammatory state of the host, and will deteriorate the maintenance of immune balance. Further influences and detailed mechanisms need to be investigated.
失血性休克可导致免疫功能障碍。调节性 T 细胞（Tregs）、辅助性 T 细胞（Th）和细胞毒性 T 淋巴细胞（CTL）在免疫和炎症反应中可发挥许多关键作用。本研究旨在探讨未进行液体复苏的控制性失血性休克大鼠外周血 CD4+CD25+Foxp3+Treg 及 Th1/Th2、Tc1/Tc2 细胞谱的早期病理生理变化。
建立未进行液体复苏的控制性失血性休克大鼠模型。于失血性休克前及无液体复苏 4 小时后采集外周血样本，采用三色流式细胞术检测样本中的 Tregs、Th1、Th2、Tc1 和 Tc2 细胞。
失血性休克后 4 小时大鼠外周血 Tregs 的百分比明显低于失血性休克前（P = 0.001）。Th1/Th2 和 Tc1/Tc2 的比值分别从（23.08 ± 8.98）%变为（23.91 ± 15.36）%和从（40.40 ± 21.56）%变为（65.48 ± 23.88）%。
在早期阶段，失血性休克的发生与 Tregs 的早期减少有关，Th1/Th2、Tc1/Tc2 平衡向 Th1 和 Tc1 优势方向发生轻微转移。这些变化是宿主过度炎症状态的一部分，将使免疫平衡的维持恶化。需要进一步研究这些变化的影响和详细机制。
