早期大剂量地塞米松对挤压综合征大鼠模型心肌特异性损伤的疗效

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摘要目的评估早期大剂量地塞米松对挤压综合征大鼠模型心肌特异性损伤的疗效。方法将Wistar大鼠随机分为4组。空白(Sham)组、对照(CS)组、生理盐水(NS)组和地塞米松(DEX)组,每组20只。CS组造模后不做任何处理;DEX组和NS组造模后在解压前即刻注射1 mg/kg地塞米松和等体积的生理盐水;Sham组对正常Wistar大鼠无造模及药物干预,行麻醉、取血和手术处理。各组收集不同时间点的血液和组织学样本。结果心肌损伤观察指标:(1)血清cTnI OD值,解压后3 h各组间差别无统计学意义。6 h时3个处理组血清cTnI均较Sham组显著上升,CS组为(0.246+0.028),NS组为(0.202+0.033),DEX 组为(0.178+0.017),差异有统计学意义(P<0.01);NS组和DEX组均低于CS组,NS组和DEX组之间差异无统计学意义。12 h时3个处理组均高于Sham组,差异有统计学意义(P<0.01);各处理组间无统计学差异。24 h时CS组和NS组高于Sham组,P<0.05;DEX组与Sham组相比差异无统计学意义;(2)心肌细胞凋亡率CS组、NS组和DEX组各时间点均高于Sham组,差异有统计学意义(P<0.01)。3 h时NS组和DEX组低于CS组,差异有统计学意义(P<0.01),NS组和DEX组间差异无统计学意义12~24 h时间段,NS组和CS组差异无统计学意义,DEX显著低于NS和CS组,差异有统计学意义(P<0.01);(3) 心肌细胞HE染色 Sham组大鼠心肌组织正常。CS组中可见充血性改变,随时间加重。NS组和DEX组充血水肿均有不同程度的减轻,DEX组减轻更明显。结论挤压综合征大鼠存在心肌细胞的特异性损伤,大剂量的地塞米松和与之等体积的生理盐水扩容均能改善这一现象,地塞米松明显优于生理盐水单纯扩容。大剂量糖皮质激素可能通过抑制全身炎性反应从而减轻挤压综合征大鼠的心肌损伤。

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关键词 ：挤压综合征, 大鼠, 炎性反应, 心肌特异性损伤, 地塞米松

Abstract：Objective To evaluate the effect of the early stage high-dose dexamethasone on cardiac-specific injury in the crush-syndrome rats.Methods CS rats were divided into three groups:CS group, NS group and DEX group (n=20 each). DEX group and NS group were intravenously administered 5mg/kg of dexamethasone and an equal volume of nomal saline respectively immediately before reperfusion while CS group received no treatment.A sham group serving as a blank control underwent the same procedures as all the three CS groups except for the compression and decompression and drug intervention. Results Myocardial specific injuries: (1) In serum cTnI OD, there were no statistically significant differences between all groups at 3 h after decompression. At 6h, the serum levels of cTnI increased in all three groups (compared with sham group), P<0.01. In NS group and DEX group were significantly lower than in CS group, and the P value was smaller than 0.05 and 0.01 respectively. There was no significant difference between DEX and NS groups. At 12 h in all three treatment groups were higher than in sham group (P<0.01).The differences between the three treatment groups were not statistically significant. At 24 h in group CS group and NS group were significantly higher than in sham group, P<0.01 and P<0.05 respectively.There was no significant difference between DEX group and sham group. In DEX group was significantly lower than in CS group, P<0.05. There were no significant differences between NS and DEX group, NS and CS group. (2) Apoptosis rate in myocardium: the apoptosis rate in CS group, NS group and DEX group at each time point were higher than that in sham group, P<0.01. At 3 h in NS group and DEX group were lower than in CS group, P<0.05 and P<0.01, respectively. There was no differences between NS and DEX group. At 6 h in NS group and DEX group were still lower than in CS group, P<0.05 and P<0.01, respectively. In DEX group were lower than in NS group, P<0.05.At 12 h and 24 h, there was no difference between NS and CS group. In DEX group were significantly lower than in NS group, P<0.01. (3) HE staining of myocardium: in sham group was normal. In the CS group, the congestive changes were observed and aggravated along with increasing time. NS group and DEX group had different degree of congestion and edema relief, and the relief in DEX group was more obvious.Conclusions There is cardiac specific injury in CS rat model, which may be threated by high-dose dexamethasone and normal saline. High-dose dexamethasone is more effective than an equal volume of normal saline. High dose of glucocorticoid may reduce the myocardial injury in crush syndrome rats through its suppression of systemic inflammatory response.

Key words： crush syndrome rats inflammation cardiac-specific injury dexamethasone

收稿日期: 2015-08-11

ZTFLH:

R514

通讯作者: 刘惠亮 E-mail: lhl518@vip.sina.com

作者简介: 於四军,博士,主治医师。

引用本文:

於四军, 严政, 路靖, 金德奎, 张聪, 刘惠亮. 早期大剂量地塞米松对挤压综合征大鼠模型心肌特异性损伤的疗效[J]. 武警医学, 2016, 27(3): 281-284. YU Sijun, YAN Zheng,LU Jing, JIN Dekui, ZHANG Cong, and LIU Huiliang. Effect of early stage high-dose dexamethasone on cardiac-specific injury in crush-syndrome rats. Med. J. Chin. Peop. Armed Poli. Forc., 2016, 27(3): 281-284.

链接本文:

http://journal08.magtechjournal.com/Jwk_wjyx/CN/ 或 http://journal08.magtechjournal.com/Jwk_wjyx/CN/Y2016/V27/I3/281

[1]	Pepe E, Mosesso V N, Falk J L, et al.Prehospital fluid resuscitation of the patient with major trauma[J]. Prehosp Emerg Care,2002,6:81-91.
[2]	Better O S. Management of shock and acute renal failure in casualties suffering from the crush syndrome[J]. Ren Fail,1997,19:647-653.
[3]	The INSARAG Medical Working Group.The medical management of the entrapped patient with crush syndrome[C].Geneva:United Nations,2011.
[4]	Isamu Murata P D, Kazuya Ooi. Acute lethal crush-injured rats can be successfully rescued by a single injection of high-dose dexamethasone through a pathway involving PI3K-Akt-eNOS signaling[J]. J Trauma Acute Care Surg,2013,75 (2):241-249.
[5]	Shuiping Liu, Yangeng Yu, Bin Luo, et al.Impact of traumatic muscle crush injury as a cause of cardiomyocyte-specific injury:an experimental study[J]. Heart Lung and Circulation,2013,22:284-290.
[6]	Murata I,Ooi K,Sasaki H,et al.Characterization of systemic and histologicinjury after crush syndrome and intervals of reperfusion in a smallanimal model [J].J Trauma,2011,70:1453-1463.
[7]	Mien Cheng Chen, Jen Ping Chang, Wan Chun Ho, et al. Expression ofspliceosome assembly factor SC-35 in TUNEL-positive atrialcardiomyocytes in mitral and tricuspid regurgitation: viability of atrial cardiomyocytes[J].Int J Cardiol,2011,151: 323-327.
[8]	Guo X,Wang D,Liu Z, et al.Electrocardiographic changes after injury in a rat model of combined crush injury. Am J Emerg Med[J]. 2013, 31:1661-5.
[9]	陈媛,周玖.自由基-炎性反应与衰老性疾病[M].北京:科学出版社,2007: 102-120.
[10]	Syed Gillani, Jue Cao, Takashi Suzuki, et al. The effect of ischemia reperfusion injury on skeletal muscleInjury[J].Int J Care Injured, 2012,43:670-675.
[11]	Nishikata R,Kato N,Hiraiwa K,et al.Oxidative stress may be involved in distant organ failure in tourniquet shock model mice[J]. Legal Medicine,2014,16:70-75.