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目的观察高渗氯化钠羟乙基淀粉溶液(hypertonic sodium chloride hydroxyethyl starch 40,HHS)对未控制出血性休克(uncontrolled hemorrhagic shock,UHS)大鼠心肌损伤的保护作用并探讨其可能机制。方法采用修订的Capone等方法制备创伤UHS模型。用随机数字表法将30只SD大鼠分为3组(n=10):正常对照组(NC组)、生理盐水复苏组(NS组)、高渗氯化钠羟乙基淀粉溶液复苏组(HHS组)。NS组及HHS组大鼠经动脉放血,使血压降至40 mmHg,然后断尾75%,造成活动性出血。分别给予生理盐水(NS)和HHS输注,使MAP维持在50 mmHg。复苏1后,两复苏组均给予手术止血、回输血液及给予足量的液体输注,保持MAP 0 mmHg。持续监测左心室收缩压(LVSP)、左室压力最大上升及下降速率(±dp/dt max)及左室舒张末压(LVEDP);分别于伤后0(T0)、30(T1)、90(T2)、210(T3)min测定肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)的活性及肌钙蛋白I(cTnI)浓度;观察实验结束时心肌组织超微结构改变;于T3时点处死大鼠,制备心肌组织匀浆,检测MDA、SOD、TNF-α及IL-6水平;经TUNEL染色观察心肌细胞凋亡情况。结果 HHS组复苏后心功能指标较NS组明显升高(P<0.05);HHS组CK-MB、LDH活性及cTnI浓度明显低于NS组(P<0.05);HHS组心肌组织超微结构损伤比NS组明显减轻;HHS组心肌匀浆MDA、TNF-α及IL-6浓度均显著低于CON组,心肌匀浆SOD活性显著高于CON组(P<0.05);HHS组大鼠心肌细胞凋亡率明显低于NS组(P<0.05)。结论 HHS对UHS大鼠心肌有保护作用;减少氧自由基释放和SOD消耗,降低炎症因子的产生以及抑制心肌细胞凋亡可能是其中的机制。
Objective To observe the protective effect of hypertonic sodium chloride hydroxyethyl starch 40 (HHS) on myocardial injury in uncontrolled hemorrhagic shock (UHS) rats and to explore its possible mechanism. Methods A modified Capone method was used to prepare the wound UHS model. Thirty SD rats were randomly divided into three groups (n = 10): normal control group (NC group), saline resuscitation group (NS group), hypertonic sodium chloride hydroxyethyl starch solution resuscitation group (HHS group). Rats in NS group and HHS group were bled by artery, blood pressure was reduced to 40 mmHg, and then tail 75%, resulting in active bleeding. Saline (NS) and HHS infusions were given respectively to maintain MAP at 50 mmHg. After recovery 1, both resuscitation groups were given surgical bleeding, blood transfusion, and adequate fluid infusion to maintain MAP 0 mmHg. Left ventricular systolic pressure (LVSP), left ventricular pressure (± dp / dt max) and left ventricular end diastolic pressure (LVEDP) were monitored continuously at 0, 0, 30 The activities of CK-MB and LDH and the concentrations of cTnI were measured at T2 and 210 (T3) min. The ultrastructure of myocardial tissue was observed at the end of the experiment The rats were sacrificed at T3, and the myocardial homogenate was prepared to detect the levels of MDA, SOD, TNF-α and IL-6. The apoptosis of cardiomyocytes was observed by TUNEL staining. Results The cardiac function indexes of HHS group after resuscitation were significantly higher than those of NS group (P <0.05). The levels of CK-MB, LDH and cTnI in HHS group were significantly lower than those in NS group (P <0.05) The level of MDA, TNF-α and IL-6 in HHS group was significantly lower than that in CON group, and the activity of SOD in myocardial homogenate was significantly higher than that in CON group (P <0.05) The apoptosis rate was significantly lower than NS group (P <0.05). Conclusion HHS can protect myocardium of UHS rats. It may be one of the mechanisms by which HHS can reduce the release of oxygen free radicals and the consumption of SOD, decrease the production of inflammatory cytokines and inhibit cardiomyocyte apoptosis.