难逆性失血性休克早期血液流变学变化的研究

目的 观察难逆性失血性休克大鼠早期血液流变学的变化特点.方法 建立失血性休克大鼠模型后,将模型大鼠随机分为4组:第1组动物观察模型制备结束后180 min内的存活情况,记录平均动脉压(MAP)和存活时间(S组).第2～4组动物均在模型制备前取血,为基础值;第2组动物在休克后0 min活杀(SO组);第3组动物在休克后60 min活杀(S1组);第4组动物在休克后120 min活杀(S2组).检测指标包括血乳酸值、全血和血浆黏度、红细胞的变形性和聚集特性.结果 S组的平均放血量为(22.9±3.8)ml/kg,约占总血量的(38.1±6.3)%.在失血性休克后60、120和180 min存活率分别为100%、72%和64%.与基础值比较,失血性休克后0、60和120 min血乳酸值明显升高(P均＜0.01),120 min较0 min降低明显(P＜0.05);休克后0 min和60 min,在剪切速率为10 s-1、60 s-1和150 s-1时全血黏度均明显降低(P均＜0.01),120 min时在剪切速率为10 s-1和60 s-1时,全血黏度明显降低(P均＜0.01);失血性休克后0、60和120 min血浆黏度及剪切速率为600 s-1、800 s-1和1 000 s-1时的红细胞变形性、红细胞聚集指数均明显降低(P均＜0.01).结论 在难逆性失血性休克早期,血乳酸值明显升高,其后有所下降,提示机体对代谢紊乱有一定的代偿和修复功能.在难逆性失血性休克后早期的不同时间点,全血黏度、血浆黏度、红细胞变形性和聚集指数均持续降低,并且在观察期内没有明显的改善.其中黏度和红细胞聚集性的变化与休克末微循环淤滞期有所不同,提示失血性休克早期救治应该纠正当时的血液流变学异常.

Hemorrheological changes in irreversible hemorrhagic shock

OBJECTIVE: To observe the characteristics of changes in hemorrheology at the early stage of irreversible hemorrhagic shock in a rodent model. METHODS: Rodent model of irreversible hemorrhagic shock was reproduced. Animals were randomized into 4 groups. In the first group, survival rate and mean arterial pressure (MAP) in 180 minutes were observed after hemorrhagic shock (S group). In the second group, animals were sacrificed soon after hemorrhagic shock (S0 group). In the third group, animals were sacrificed 60 minutes after hemorrhagic shock (S1 group). In the fourth group, animals were sacrificed 120 minutes after hemorrhagic shock (S2 group). Blood samples of animals of S0, S1 and S2 were all obtained before hemorrhagic shock. Blood lactate, hemorheological parameters, red blood cell (RBC) deformability and RBC aggregation index were determined. RESULTS: Mean blood loss of S group was (22.9+/-3.8) ml/kg, constituting about (38.1+/-6.3)% of total blood volume. At 60, 120 and 180 minutes after hemorrhagic shock, survival rates were 100%, 72% and 64%, respectively. Compared with baseline, 0, 60 and 120 minutes after hemorrhagic shock, blood lactate increased significantly (all P<0.01), but 120 minutes after hemorrhagic shock, it decreased significantly compared with 0 minute after hemorrhagic shock (P<0.05). Compared with baseline, 0 minute and 60 minutes after hemorrhagic shock, blood viscosity was found to be decreased at shear rate of 10 s(-1), 60 s(-1) and 100 s(-1) (all P<0.01); 120 minutes after hemorrhagic shock, at shear rate of 10 s-1 and 60 s(-1), blood viscosity decreased significantly (both P<0.01); 0, 60 and 120 minutes after hemorrhagic shock, plasma viscosity, RBC deformability and RBC aggregation index at shear rates of 600 s(-1), 800 s(-1) and 1 000 s(-1) decreased significantly (all P<0.01). CONCLUSION: At the early stage of irreversible hemorrhagic shock, blood lactate increased significantly, and decreased afterwards. These indicate reversal of deterioration of metabolism. At different time after the early stage of irreversible hemorrhagic shock, blood and plasma viscosity, RBC deformability and aggregation index lowered significantly and did not improve. Changes in viscosity and RBC aggregation are different from the changes in late stage, and this indicates that hemorheological disorders should be corrected in the treatment at the early stage after hemorrhagic shock.