高渗氯化钠羟乙基淀粉40对猪脑外伤并失血性休克后脑灌注的影响

目的 观察高渗氯化钠羟乙基淀粉40（HSH40）对猪脑外伤并失血性休克后脑灌注的影响。方法 12只实验用小型猪在麻醉镇静、机械通气下，采用脑额叶气击伤、硬膜外球囊及股动脉放血的方法，建立脑外伤急性颅高压并失血性休克模型。建模后稳定1 h，将12只动物随机分入三组（n=4），分别静脉输注等失血量的羟乙基淀粉200/0.5（HES组）、20%失血量的7.5%高渗氯化钠注射液（HS组）、35%失血量的HSH40注射液（HSH组）。观察建模前（T01）、建模后60 min 即复苏处理前（T0）、复苏处理后15 min（T15）、30 min(T30)、60 min(T60)、120 min(T120)、180 min(T180)时平均动脉压（MAP）、颅内压（ICP）、脑灌注压（CPP）的变化；同时观察T01、T0、T15、T60、T120五个时点的血钠、血浆渗透压（OSM）、动静脉血氧含量差（Da-jvO2）、氧摄取率（OER）的变化。结果 与复苏处理前（T0）比较，各组复苏处理后MAP均明显上升，HSH组上升速度最快；达峰后，HSH组和HES组MAP呈缓慢下降趋势；而HS组MAP则下降迅速。HSH组和HS组复苏处理后各时点ICP较T0均明显降低(P<0.05)；复苏处理后，HES组各时点ICP均高于T0，除T15外的各时点ICP与T0比较，差异均有统计学意义(P<0.05)。复苏处理后，各组CPP均迅速上升,达峰后下降，各时点CPP均明显高于T0（P<0.05）；HSH组、HS组CPP的上升速度快于HES组；HSH组CPP在复苏处理后各时点均高于HES组（P<0.05），达峰后明显高于HS组（P<0.05）。各组Da-jvO2和OER在T0时较T01时增大（P<0.05），复苏处理后各时点较T0时降低（P<0.05）；HS组和HSH组的OER于T60降至T01水平（P>0.05），但HS组T120时的OER又高于T01（P<0.05）。HSH组、HS组复苏处理后各时点的血Na+浓度和OSM较T0均明显升高（P<0.05），峰值出现于T15。结论 小剂量（约6.6 mL/kg）HSH40在有效纠正猪脑外伤合并失血性休克MAP的同时，可以降低升高的ICP，提升CPP，恢复性增加脑血流量，改善脑氧供需平衡。

Effects of hypertonic sodium chloride hydroxyethyl starch 40 on cerebral perfusion of pigs with traumatic brain injury and hemorrhagic shock

Objective To investigate the effects of hypertonic sodium chloride hydroxyethyl starch 40 (HSH40) on cerebral perfusion of pigs with traumatic brain injury (TBI) and hemorrhagic shock. Methods Models of TBI, acute intracranial hypertension and hemorrhagic shock were established in 12 miniature pigs under anesthesia and mechanical ventilation by controlled cortical impact, epidural balloon method and blood withdrawal via femoral artery. One hour after model establishment, animals were divided into three groups (n=4), and were intravenously infused with hydroxyethyl starch 200/0.5 (HES group, equivalent volume of removed blood), hypertonic saline 7.5% (HS group, 20% volume of removed blood) and HSH40 (HSH group, 35% volume of removed blood), respectively. Physiological data, including mean arterial pressure(MAP), intracranial pressure(ICP) and cerebral perfusion pressure (CPP) were observed before model establishment(T01), 60 min after model establishment (before resuscitation)(T0) and 15 min(T15), 30 min(T30), 60 min(T60), 120 min(T120) and 180 min(T180) after resuscitation. Besides, changes of serum sodium, plasma osmotic pressure(OSM), arteriovenous oxygen difference (Da-jvO2) and cerebral oxygen enhancement ratios (OER) of T01, T0, T15, T60 and T120 were observed. Results After resuscitation treatment, MAP in each group significantly increased (P<0.05), and the increase in HSH group was the fastest. After reaching the peak, MAP in HSH group and HES group slowly decreased, while MAP in HS group decreased fast. After resuscitation treatment, ICP in HSH group and HS group of each time point decreased significantly (P<0.05), whereas an elevated ICP occurred in HES group (P<0.05 except for T15). After resuscitation treatment, CPP in each group increased fast, and decreased after reaching the peak, with CCP of each time point significantly higher than those of T0 (P<0.05). CPP in HSH group and HS group increased faster than that in HES group, with HSH group higher than HES group at each time point after resuscitation treatment (P<0.05) and higher than HS group after reaching the peak (P<0.05). Da-jvO2 and OER of T0 in each group were significantly higher than those of T01 (P<0.05), and Da-jvO2 and OER of time points after resuscitation treatment were significantly lower than those of T0 (P<0.05). OER in HS group and HSH group of T60 decreased to those of T01 (P>0.05), while OER of T120 was significantly higher than that of T01 in HS group (P<0.05). Serum sodium and OSM of each time point after resuscitation treatment were significantly higher than those of T0 in HSH group and HS group (P<0.05), and the peak values reached at T15. Conclusion HSH40 (6.6 mL/kg) can effectively resuscitate MAP, reduce ICP, increase CCP and cerebral blood flow, and improve the balance of supply and demand of cerebral oxygen of pigs with TBI and hemorrhagic shock.