摘要
目的 研究挤压伤后多器官功能障碍综合征(MODS)的发病机制和预防方法。
方法 (1)制做挤压伤后多器官功能障碍综合征的家兔实验模型。用32kg重物挤压家兔双后肢大腿和臀部，根据挤压时间不同可分为挤压4h组20只和挤压5h组20只，另设正常对照组10只。解除挤压24h后，取血液测定血细胞比积(Hct)、血小板计数，血浆谷丙转氨酶(GPT)、肌酐(Cr)、蛋白含量和支气管肺泡灌洗液蛋白含量，用以代表器官功能的状况；并观察肺、肝、肾、胃肠道及大腿肌群病理变化。(2)研究挤压伤后多器官功能障碍综合征的发病机制和防治方法。用32kg重物挤压家兔大腿和臀部5h，作为挤压伤的模型，分别于挤压前和解压前给药，根据给药不同，把动物分成生理盐水组(NS组，10只)、辅酶Q_(10)组(CoQ_(10)组，8只)、甘露醇组(Mannitol组，9只)和维生素C组(VitC组，9只)，另设正常对照组(对照组，10只)。观测解压后2h内的平均动脉压和24h血浆NAG、SOD、MDA和NO含量的动态变化和组织MDA、NO含量变化，并观测解压后24h时反映器官功能的指标和相应的组织病理学变化。
结果 (1)挤压5h组在解压后2h内，平均动脉压均比挤压4h组低(P＜0.05)，多系统器官衰竭(MSOF)的发生率为60.0％，比挤压4h组的35.0％高(但经X~2检验，P＞0.05，差异无显著性)，器官衰竭发生率高的排列，依次为肝、肾、肺、小肠、凝血系统；压伤5h组为Hct 55.6％±13.0％，而压伤4h组为48.5％±11.4％，两组比较无显著性差异；压伤5h组组织细胞的损伤变化普遍比压伤4h组严重。(2)CoQ_(10)、Mannitol、VitC三治疗组同NS组比较：解压后2h内平均动脉压明显升高(P＜0.05)，血浆NAG、MDA和NO含量在解压后24h动态变化中亦明显降低(P＜0.05)，而血浆SOD于解压后2h至24h间表现出明显增高(P＜0.05)。各治疗组解压后24h时组织MDA和NO含量均比NS组有不同程度的降氐，但比对照
安l救医科大学硕士学位论文
组亦有不同程度的增高。CoQI。、Manni tol、VitC三组的破刃F的发生率分别为
25.以、33.3%、33.3%，比NS组的60.既低，但无统计学差异;各单器官衰竭的
发生率亦均低J几NS组;在各治疗组中，反映肾脏细胞损伤的尿NAG、肺脏损伤
的肺卿重指数和血液粘稠度的Ilct所表现出均低于NS组(P<0.05)。光镜下实验
组，卜各细胞均仃不同程度的损伤性变化，其中以NS组损伤最为严重，而三治疗
组相对较轻。三组之间各种指标变化差异不大。
结论(l)32kg重物挤压家兔双后肢大腿和臀部5h解除挤压后，可以制做出挤
压伤后沁[)S的实验动物模型。(2)挤压伤后引起MODS，其发病机制可能由于缺
血再灌注损伤造成的，而大量的自山基产生，可以引起细胞、组织乃至系统、器
官功能的损害，在缺血前或/和再灌注前应用抗自由基的药物，能起到防治挤压
伤后M()l)片「!勺f乍川。
Objective The study of mechanism and experimental treatment in multiple organ dysfunction syndrome (MODS) after crush injury.
Methods (1) It was reproduced that an animal model of multiple organ dysfunction syndrome after crush injury in rabbits. The hindlimbs were crushed by 32 kg weight of stone for 4 hours or 5 hours in rabbits. It was grouped as crush 4 hours group (n=20), crush 5 hours (n=20) and normal group (n=10). Hematocrit (Hct)-. thrombocyte, glutamic-pyruvic transaminase(GPT) and creatinine(Cr) in blood were determined in 24 hour after crush injury. Protein contents in plasma and in broncho-alveolus lavage fluid (BALF) were determinedCells in hu^ liven kidney ^ intestine and skeletal muscle tissue were observed under microscope in 24 hour after crush injury. (2) The study of mechanism and experimental treatment in multiple organ dysfunction syndrome after crush injury. It was reproduced that an animal model of multiple organ dysfunction syndrome after crush injury by 32 kg for 5 hours in rabbits and injected by drugs in vein before and after crush injury respectively. It was grouped as CoQ10 group(n=8), mannitol group (
n=9), VitC group (n=9), normal saline (NS) group (n=10), normal group (n=10). The arteral blood pressure were determined within 2 hours after crush injury. N-acetyl- P -D-glucosaminidase (NAG) -. superoxide dismutase (SOD) , malondialdehyde (MDA)> nitric oxide (NO) in plasma and MDA-. NO in heart, lung., liver, kidney , intestine and skeletal muscle tissue were determined GPT and Cr in plasma-, protein in BALF/plasma, NAG in urinal were studied in 24 hour after crush injury. Cells in heart, lung, liver, kidney, intestine and skeletal muscle tissue in all
groups were observed under microscope in 24 hour after crush injury.
Results (1) The arteral blood pressure in crush 5h group was greater than that in crush 4h group within 2 hours after crush injury (p<0.05). The incidence of multiple system organ failure (MSOF) in crush 5h group was 60.0% vs in crush 4h group 35.0% (p>0.05). The percentage of liver, kidney, lung, intestine and coagulation system failure was respectively 60.0%, 55.0%, 40.0%, 30.0% and 25.0%. Hct was 55.6%?3.0% in crush 5h group and 48.5%?1.4% in crush 4h group (p>0.05). There were cells injury in two groups in 24 hour after crush injury. (2) The arteral blood pressure in treatment groups was higher than that in NS group during 2 hours after crush injury (p<0.05). The contents of NAG, MDA, NO in plasma in treatment groups were signicantly lower than those in NS group during 24 hours after crush injury (p<0.05),but SOD activity in plasma in treatment groups higher those in NS group within 2 to 24 hours after crush injury (p<0.05). The contents of MDA and NO in heart, lung, liver, kidney, intestine and skeletal muscle tissue in treatment groups were lower than those in NS group but higher than those in normal group. The incidence of MSOF in CoQ10, mannitol and VitC groups was respectively 25.0%, 333%, 333%, but 60.0% in NS group. NAG in urinal, protein in BALF/plasma-, Hct in treatment groups was lower than those in the NS group in 24 hour after crush injury (p<0.05). crush injury may induce cellular injury in heart, lung, liver, kidney, intestine and skeletal muscle tissues in 24 hour after crush injury but cellular injury was reduced by CoQ10, mannitol and VitC treatment.
Conclusion (1) The animal model of MODS after crush injury was reproduced that the hindlimbs in rabbits were crushed by 32 kg weight of stone for 5 hours. (2) MODS after crush injury was induced by ischemia reperfusion injury. Free redicals in ischemia reperfusion injury play an important role in organ, tissue and celluar injury. Using free
radical scavengers before ischemic or , and reperfusion, such as coenzyme Q10, mannilol, vitamin C, can precaution and treat MODS after crush injury before ischemic
or , and reperfusion.
引文
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