Sullivan D J, Barton R G, Edelman L S, Shao Y, Nelson E W, Shelby J
Department of Surgery, University of Utah, School of Medicine, Salt Lake City 84132, USA.
J Surg Res. 1998 Feb 15;75(1):54-60. doi: 10.1006/jsre.1997.5254.
Allogeneic blood transfusion is known to be immunosuppressive in the settings of cancer and transplantation, but the contribution of blood transfusion to immunomodulation after hemorrhage is unknown. Our purpose was to determine the influence of allogeneic blood transfusion upon cytokine profiles following hemorrhagic shock, using a model which approximates the clinical setting.
Male C3H/HeN mice were hemorrhaged via femoral arterial catheters to a mean arterial pressure (MAP) of 35 +/- 5 mm Hg, which was maintained for 1 h. Mice were resuscitated with autologous blood (auto BT) or allogeneic blood (allo BT) from Balb/c mice (both equivalent to volume of shed blood), and crystalloid (2X the volume of shed blood)-infused at 0.05 ml/min. Animals were sacrificed at 1, 2, and 5 days postshock, and splenocytes were cultured for 24 h with anti-CD3 antibody. Supernatants were assayed for IL-2, IL-6, IL-10, and gamma-IFN by ELISA.
Regardless of transfusion status, hemorrhagic shock resulted in increased IL-6 and gamma-IFN by Day 2 postshock. Distinct cytokine alterations after allogeneic transfusion were as follows. IL-2: transient elevation of splenocyte IL-2 production in the shock + allo BT group (P < 0.005 vs. shock + auto BT) at Postshock Day 2. IL-6: suppression in IL-6 production in the shock + allo BT group by Postshock Day 5 (P < 0.05 vs. shock + auto BT). IL-10: persistently elevated IL-10 production following shock + allo BT (Day 1, P < 0.001 vs. shock + auto BT; Day 5; P < 0.05 vs. shock + auto BT). gamma-IFN: elevation in gamma-IFN production by Day 5 in the shock + allo BT group (P < 0.0005 vs. shock + auto BT).
Allogeneic blood transfusion results in distinct alterations in splenocyte production of IL-2, IL-6, IL-10, and gamma-IFN after hemorrhagic shock. This model reflects the clinical usage of blood products and demonstrates some of the immune alterations after transfusion.
已知同种异体输血在癌症和移植情况下具有免疫抑制作用，但输血对出血后免疫调节的作用尚不清楚。我们的目的是使用一个近似临床情况的模型来确定同种异体输血对失血性休克后细胞因子谱的影响。
通过股动脉导管将雄性C3H/HeN小鼠放血至平均动脉压（MAP）为35±5 mmHg，并维持1小时。用来自Balb/c小鼠的自体血（自体输血）或同种异体血（异体输血）（两者均相当于失血量）对小鼠进行复苏，并以0.05 ml/min的速度输注晶体液（失血量的2倍）。在休克后1、2和5天处死动物，并将脾细胞与抗CD3抗体一起培养24小时。通过酶联免疫吸附测定法检测上清液中的白细胞介素-2（IL-2）、白细胞介素-6（IL-6）、白细胞介素-10（IL-10）和γ-干扰素（γ-IFN）。
无论输血状态如何，失血性休克在休克后第2天导致IL-6和γ-IFN增加。同种异体输血后不同的细胞因子变化如下。IL-2：休克+异体输血组在休克后第2天脾细胞IL-2产生短暂升高（与休克+自体输血组相比，P<0.005）。IL-6：休克+异体输血组在休克后第5天IL-6产生受到抑制（与休克+自体输血组相比，P<0.05）。IL-10：休克+异体输血后IL-10产生持续升高（第1天，与休克+自体输血组相比，P<0.001；第5天，与休克+自体输血组相比，P<0.05）。γ-IFN：休克+异体输血组在第5天γ-IFN产生升高（与休克+自体输血组相比，P<0.0005）。
同种异体输血导致失血性休克后脾细胞产生的IL-2、IL-6、IL-10和γ-IFN发生明显改变。该模型反映了血液制品的临床使用情况，并证明了输血后一些免疫改变。
