兔后肢挤压伤的磁共振定量评价及缺血后处理效果研究
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摘要
目的
横纹肌溶解症主要是由于骨骼肌细胞坏死导致细胞内容物进入细胞外液和循环中,进而导致一系列威胁生命的并发症。横纹肌溶解的病因包括药物、感染、高强度运动、肌肉疾病及挤压伤。挤压伤所致者亦称为创伤性横纹肌溶解症,常见于地震、飓风等自然灾害中的受伤者。挤压伤常并发致命的并发症,包块严重的电解质紊乱、低血容量性休克、肾衰竭等,因此早期诊断非常重要。除了实验室检查外,影像学检查也可以提供非常有用的诊断信息,尤其是在确定病变的范围和程度方面具有优势。磁共振成像(magnetic resonance imaging,MRI)具有较高的灵敏度和很好的软组织分辨率,被认为是评价创伤性横纹肌溶解的最佳影像学检查方法之一。但由于临床病例很难获得肌肉标本,进行病理组织学检查较困难,因此MRI表现与病理学改变的关系尚不明确。同时,随着MRI技术的不断进步,定量诊断在临床运用亦日渐普遍,但在挤压伤的诊断领域尚未见报告。本实验通过比较兔后肢挤压伤的MRI指标动态变化与肌肉病理学改变的相关性,明确探讨T2WI信号变化的病理学基础;同时评估兔后肢挤压伤MRI定量测定的临床诊断价值。另外,在肢体挤压伤的现场救治中,降低缺血再灌注的损害亦十分重要。缺血后处理是近年来新提出的通过调动机体内源性保护机制减轻组织器官缺血再灌注损伤的新措施,已有研究证实,缺血后处理能供有效防止大鼠缺血性急性肾衰竭。而且缺血后处理在现场救治中比缺血预处理更具有可操作性。本研究首次运用缺血后处理方式处理受挤压肢体,探讨该措施对肠道屏障的保护及对全身炎症反应综合征(systemic inflammatory response syndrome,SIRS)的抑制作用,为肢体挤压伤的现场救治提供实验依据。
方法
1.建立兔后肢挤压伤模型并在第1、3、7、14及30d分别进行MRI(T1WI,T2WI,T2map)、肌肉病理学、血浆肌肉肌钙蛋白(muscular troponin,sTnI)值及尿液肌红蛋白(myoglobin,Myo)检查,探讨影像学指标与病理生理学变化之间的相关性。
2.建立兔后肢挤压伤模型并分别采取两种缺血后处理方式:交替夹闭-开放挤压伤侧髂总动静脉(group of ischemic postconditioning-A,IP-A组,每次60s,反复3次);交替捆绑-松弛挤压伤肢体近端(group of ischemic postconditioning-B IP-B组,每次60s,反复3次)。检测处理前、处理后2、6、12、24h后血浆二胺氧化酶(diamine oxidase,DAO)及肠脂肪酸结合蛋白(intestinal fatty acid-binding protein,iFABP)水平,24h后取回肠组织HE染色观察肠粘膜形态学改变,探讨这两种缺血后处理方式对后肢挤压伤兔肠道屏障的保护作用。
3.建立兔后肢挤压伤模型及以两种缺血后处理方式处理后肢挤压伤兔,检测IP-A组及IP-B组处理前、处理后2、6、12、24h后血浆白介素-6(interleukin-6,IL-6)、白介素-10(interleukin-10,IL-10)及肿瘤坏死因子-α(tumor necrosis factorα,TNF-α)水平,比较两种处理方式组及对照组上述指标的变化,探讨这两种缺血后处理方式对后肢挤压伤兔全身炎症反应综合征的抑制作用。
结果
1.挤压伤后第1、3及7d,受损肌肉的T2WI呈高信号,T2值持续上升;肌肉病理显示细胞水肿破裂、细胞外间隙扩大、炎症反应及细小肌纤维再生;血清sTnI值、尿液Myo值亦维持较高水平。第14d后,上述各项指标均逐步趋于正常。T2WI的改变、T2值与肌肉病理改变、血清sTnI值及尿液Myo值变化呈正相关;而各时间点T1WI信号变化不明显。
2.IP-A组与IP-B组在上述处理后2、6、12、24h时相点血浆iFABP水平均低于对照组(p<0.05);处理后2、6h血浆DAO水平均低于对照组(p<0.05);两种缺血后处理模式组间差异无统计学意义;各组肠粘膜在形态上未见明显差异。
3.IP-A组与IP-B组在上述处理后2、6、12、24h时相点IL-6及TNF-α水平均低于对照组(p<0.05),处理后2、6、12h血浆IL-10水平高于对照组(p<0.05);但两种“缺血后处理”模式组间无差别(p>0.05)。
结论
1.挤压伤后受损肌肉MRI检查的T2WI信号及T2值的改变与病理改变及血浆sTnI、尿液Myo浓度具有正相关性,表明T2WI信号及T2值的检测可敏感评价兔后肢挤压伤的伤情。T2WI的高信号及T2值增加可能与受损伤肌组织胞外间隙的扩大、局部的炎症反应及肌纤维的不完全再生有关。
2.缺血后处理对兔后肢挤压伤早期肠道屏障有保护作用,表现为处理后血浆iFABP水平及DAO水平均低于对照组;肠粘膜形态修复早于肠屏障功能的恢复。缺血后处理对兔后肢挤压伤早期全身炎症反应有抑制作用,表现为处理后血浆IL-6及TNF-α水平均低于对照组,IL-10水平高于对照组。本研究结果提示缺血后处理可能作为肢体挤压伤后救治的新策略。
Objective
Rhabdomyolysis refers to life threatening complications caused by the necrosis of skeletal muscles and the subsequent entry of the intracellular content into the extracellular fluid and circulation. Traumatic Rhabdomyolysis refers to Rhabdomyolysis caused mainly by crush injury,which is common during natural disasters such as earthquake and hurricane. Laboratory investigations indicate an increased plasma creatine kinase and urine myoglobin. However,in the early stage of the disease,the clinical symptoms may be subtle and easily missed. And laboratory findings are easily neglected in the early phase of the illness. Since the complications of the Rhabdomyolysis are life threatening,it is vital to make an early diagnosis and institute early interventions. In addition to laboratory examination, imaging techniques can provide very useful information,especially,in terms of the severity and range of the lesion. Magnetic Resonance Imaging (MRI) has good sensitivity and soft tissue resolution and is considered to be the best imaging modality in evaluating Traumatic Rhabdomyolysis. But it is difficult to obtain muscle samples from clinical cases of rhabdomyolysis, the correlation between MRI and muscle histopathology is indefinite. The present study is a comparison between the association of dynamic changes of rabbit crush injury MRI images and the pathological changes of the muscle to confirm the pathological basis of the T2WI signal changes. Furthermore,in the study,the changes of T2 values were quantitatively measured with T2 mapping technique and then compared with muscular injury indices such as serum troponin (sTnI) and urine myoglobin (Myo) to evaluate the clinical importance of quantitative MRI technique. And in the field first aid of crush injury,it is important to decrease the damage of ischemia-reperfusion. Ischemic postconditioning (IP) is a new measure raised recently to decrease the damage of ischemia-reperfusion. Some reports have proved that IP could prevent acute ischemic renal failure in rats. But there are few reports in the field first aid of crush injury. This study is to explore Inhibition of Ischemic Postconditioning to systemic inflammatory response syndrome (SIRS) and intestinal mucosa barrier protective effects by two types of ischemic postconditioning on the model of hind limb crush injury in rabbits.
Methods
1. We established a rabbit hind limb crush injury model and performed examinations on MRI (T1WI, T2WI and T2 map), muscle pathology, serum level of muscular troponin (sTnI) and urine myoglobin (Myo) at 1, 3, 7, 14 and 30 days after injury to investigate the correlation among MRI, library examination and histopathology.
2. A rabbit hind limb crush injury model and two types of ischemic postconditioning in the models,i.e,IP-A:occlusion/open alternately (60s/time,3times) common iliac artery and vein and IP-B:bind/ loosen alternately (60s/time,3times) the proximum of the injury hind limb were established,and then some data were performed examinations including serum level of diamine oxidase (DAO) and intestinal fatty acid-binding protein (iFABP) at 2,6,12 and 24h after injury, furthermore performed examinations on the pathological changes of ileum at 24h after injury.
3. A rabbit hind limb crush injury model and two types of ischemic postconditioning in the models,i.e,IP-A:occlusion/open alternately (60s/time,3times) common iliac artery and vein and IP-B:bind/ loosen alternately (60s/time,3times) the proximum of the injury hind limb were established , and then performed examinations on serum level of interleukin-6 (IL-6),interleukin-10(IL-10)and tumor necrosis factorα(TNF-α) at 2h,6h,12h and 24h after injury.
Results
1. T2WI of the injured muscle showed high signal intensity at 1,3 and 7 days after crush injury and the T2 value continued to rise. The pathological findings of the muscle included swollen and ruptured cells,expanded extra-cellular space, inflammatory reactions and fine muscle fiber regeneration. The serum sTnI and urine Myo were high. At 14 days,these indices returned to normal gradually. The T2WI changes and T2 value were positively associated with the pathological changes of the muscles,serum sTnI and urine Myo changes. However,the signal intensity of T1WI did not vary significantly at different time points.
2. The serum levels of iFABP at 2,6,12h and 24h after injury in two groups of ischemic postconditioning were respectively IP-A : 108.75±4.81 , 117.04±3.70 ,125.52±4.22,109.12±6.95ng/ml and IP-B:108.62±3.05,117.83±3.45,127.93±3.86,106.59±3.92ng/ml.There was a significant descent compared with those in the control group. And also there was a significant descent in serum level of DAO at 2h and 6h after injury in two groups (I-post A:7.48±0.46,8.69±0.69U/ml,I-post B:7.43±0.46,8.70±0.70U/ml) compared with those in the control group(p<0.05).But there was no difference between the two groups of ischemic postconditioning. There was no difference in the pathological changes of ileum among all the group.
3. There was a significant descent in serum level of IL-6 and TNF-αat 2h,6h,12h and 24h after injury in two groups of ischemic postconditioning,and a significant increase in serum level of IL-10 at 2h,6h and 12h after injury in two groups to the control group(p<0.05).But there was no difference between the two groups of ischemic postconditioning(p>0.05).
Conclusions
1. T2WI and T2 value from T2 mapping are very useful methods of choice to evaluate the distribution and extension of the affected muscles. The high signal intensity on T2WI of the affected muscles after crush injury may be due to an increased extracellular space,local inflammation and incomplete muscle fiber regeneration.
2. Ischemic postconditioning can protect intestinal mucosa barrier on the model of hind limb crush injury in rabbits. The morphological restoration of intestinal mucosa is earlier than the function recovery of intestinal mucosa barrier.Ischemic postconditioning can inhibition SIRS on the model of hind limb crush injury in rabbits. This study shows that ischemic postconditioning may be a new way to treat limb crush injury.
横纹肌溶解症主要是由于骨骼肌细胞坏死导致细胞内容物进入细胞外液和循环中,进而导致一系列威胁生命的并发症。横纹肌溶解的病因包括药物、感染、高强度运动、肌肉疾病及挤压伤。挤压伤所致者亦称为创伤性横纹肌溶解症,常见于地震、飓风等自然灾害中的受伤者。挤压伤常并发致命的并发症,包块严重的电解质紊乱、低血容量性休克、肾衰竭等,因此早期诊断非常重要。除了实验室检查外,影像学检查也可以提供非常有用的诊断信息,尤其是在确定病变的范围和程度方面具有优势。磁共振成像(magnetic resonance imaging,MRI)具有较高的灵敏度和很好的软组织分辨率,被认为是评价创伤性横纹肌溶解的最佳影像学检查方法之一。但由于临床病例很难获得肌肉标本,进行病理组织学检查较困难,因此MRI表现与病理学改变的关系尚不明确。同时,随着MRI技术的不断进步,定量诊断在临床运用亦日渐普遍,但在挤压伤的诊断领域尚未见报告。本实验通过比较兔后肢挤压伤的MRI指标动态变化与肌肉病理学改变的相关性,明确探讨T2WI信号变化的病理学基础;同时评估兔后肢挤压伤MRI定量测定的临床诊断价值。另外,在肢体挤压伤的现场救治中,降低缺血再灌注的损害亦十分重要。缺血后处理是近年来新提出的通过调动机体内源性保护机制减轻组织器官缺血再灌注损伤的新措施,已有研究证实,缺血后处理能供有效防止大鼠缺血性急性肾衰竭。而且缺血后处理在现场救治中比缺血预处理更具有可操作性。本研究首次运用缺血后处理方式处理受挤压肢体,探讨该措施对肠道屏障的保护及对全身炎症反应综合征(systemic inflammatory response syndrome,SIRS)的抑制作用,为肢体挤压伤的现场救治提供实验依据。
方法
1.建立兔后肢挤压伤模型并在第1、3、7、14及30d分别进行MRI(T1WI,T2WI,T2map)、肌肉病理学、血浆肌肉肌钙蛋白(muscular troponin,sTnI)值及尿液肌红蛋白(myoglobin,Myo)检查,探讨影像学指标与病理生理学变化之间的相关性。
2.建立兔后肢挤压伤模型并分别采取两种缺血后处理方式:交替夹闭-开放挤压伤侧髂总动静脉(group of ischemic postconditioning-A,IP-A组,每次60s,反复3次);交替捆绑-松弛挤压伤肢体近端(group of ischemic postconditioning-B IP-B组,每次60s,反复3次)。检测处理前、处理后2、6、12、24h后血浆二胺氧化酶(diamine oxidase,DAO)及肠脂肪酸结合蛋白(intestinal fatty acid-binding protein,iFABP)水平,24h后取回肠组织HE染色观察肠粘膜形态学改变,探讨这两种缺血后处理方式对后肢挤压伤兔肠道屏障的保护作用。
3.建立兔后肢挤压伤模型及以两种缺血后处理方式处理后肢挤压伤兔,检测IP-A组及IP-B组处理前、处理后2、6、12、24h后血浆白介素-6(interleukin-6,IL-6)、白介素-10(interleukin-10,IL-10)及肿瘤坏死因子-α(tumor necrosis factorα,TNF-α)水平,比较两种处理方式组及对照组上述指标的变化,探讨这两种缺血后处理方式对后肢挤压伤兔全身炎症反应综合征的抑制作用。
结果
1.挤压伤后第1、3及7d,受损肌肉的T2WI呈高信号,T2值持续上升;肌肉病理显示细胞水肿破裂、细胞外间隙扩大、炎症反应及细小肌纤维再生;血清sTnI值、尿液Myo值亦维持较高水平。第14d后,上述各项指标均逐步趋于正常。T2WI的改变、T2值与肌肉病理改变、血清sTnI值及尿液Myo值变化呈正相关;而各时间点T1WI信号变化不明显。
2.IP-A组与IP-B组在上述处理后2、6、12、24h时相点血浆iFABP水平均低于对照组(p<0.05);处理后2、6h血浆DAO水平均低于对照组(p<0.05);两种缺血后处理模式组间差异无统计学意义;各组肠粘膜在形态上未见明显差异。
3.IP-A组与IP-B组在上述处理后2、6、12、24h时相点IL-6及TNF-α水平均低于对照组(p<0.05),处理后2、6、12h血浆IL-10水平高于对照组(p<0.05);但两种“缺血后处理”模式组间无差别(p>0.05)。
结论
1.挤压伤后受损肌肉MRI检查的T2WI信号及T2值的改变与病理改变及血浆sTnI、尿液Myo浓度具有正相关性,表明T2WI信号及T2值的检测可敏感评价兔后肢挤压伤的伤情。T2WI的高信号及T2值增加可能与受损伤肌组织胞外间隙的扩大、局部的炎症反应及肌纤维的不完全再生有关。
2.缺血后处理对兔后肢挤压伤早期肠道屏障有保护作用,表现为处理后血浆iFABP水平及DAO水平均低于对照组;肠粘膜形态修复早于肠屏障功能的恢复。缺血后处理对兔后肢挤压伤早期全身炎症反应有抑制作用,表现为处理后血浆IL-6及TNF-α水平均低于对照组,IL-10水平高于对照组。本研究结果提示缺血后处理可能作为肢体挤压伤后救治的新策略。
Objective
Rhabdomyolysis refers to life threatening complications caused by the necrosis of skeletal muscles and the subsequent entry of the intracellular content into the extracellular fluid and circulation. Traumatic Rhabdomyolysis refers to Rhabdomyolysis caused mainly by crush injury,which is common during natural disasters such as earthquake and hurricane. Laboratory investigations indicate an increased plasma creatine kinase and urine myoglobin. However,in the early stage of the disease,the clinical symptoms may be subtle and easily missed. And laboratory findings are easily neglected in the early phase of the illness. Since the complications of the Rhabdomyolysis are life threatening,it is vital to make an early diagnosis and institute early interventions. In addition to laboratory examination, imaging techniques can provide very useful information,especially,in terms of the severity and range of the lesion. Magnetic Resonance Imaging (MRI) has good sensitivity and soft tissue resolution and is considered to be the best imaging modality in evaluating Traumatic Rhabdomyolysis. But it is difficult to obtain muscle samples from clinical cases of rhabdomyolysis, the correlation between MRI and muscle histopathology is indefinite. The present study is a comparison between the association of dynamic changes of rabbit crush injury MRI images and the pathological changes of the muscle to confirm the pathological basis of the T2WI signal changes. Furthermore,in the study,the changes of T2 values were quantitatively measured with T2 mapping technique and then compared with muscular injury indices such as serum troponin (sTnI) and urine myoglobin (Myo) to evaluate the clinical importance of quantitative MRI technique. And in the field first aid of crush injury,it is important to decrease the damage of ischemia-reperfusion. Ischemic postconditioning (IP) is a new measure raised recently to decrease the damage of ischemia-reperfusion. Some reports have proved that IP could prevent acute ischemic renal failure in rats. But there are few reports in the field first aid of crush injury. This study is to explore Inhibition of Ischemic Postconditioning to systemic inflammatory response syndrome (SIRS) and intestinal mucosa barrier protective effects by two types of ischemic postconditioning on the model of hind limb crush injury in rabbits.
Methods
1. We established a rabbit hind limb crush injury model and performed examinations on MRI (T1WI, T2WI and T2 map), muscle pathology, serum level of muscular troponin (sTnI) and urine myoglobin (Myo) at 1, 3, 7, 14 and 30 days after injury to investigate the correlation among MRI, library examination and histopathology.
2. A rabbit hind limb crush injury model and two types of ischemic postconditioning in the models,i.e,IP-A:occlusion/open alternately (60s/time,3times) common iliac artery and vein and IP-B:bind/ loosen alternately (60s/time,3times) the proximum of the injury hind limb were established,and then some data were performed examinations including serum level of diamine oxidase (DAO) and intestinal fatty acid-binding protein (iFABP) at 2,6,12 and 24h after injury, furthermore performed examinations on the pathological changes of ileum at 24h after injury.
3. A rabbit hind limb crush injury model and two types of ischemic postconditioning in the models,i.e,IP-A:occlusion/open alternately (60s/time,3times) common iliac artery and vein and IP-B:bind/ loosen alternately (60s/time,3times) the proximum of the injury hind limb were established , and then performed examinations on serum level of interleukin-6 (IL-6),interleukin-10(IL-10)and tumor necrosis factorα(TNF-α) at 2h,6h,12h and 24h after injury.
Results
1. T2WI of the injured muscle showed high signal intensity at 1,3 and 7 days after crush injury and the T2 value continued to rise. The pathological findings of the muscle included swollen and ruptured cells,expanded extra-cellular space, inflammatory reactions and fine muscle fiber regeneration. The serum sTnI and urine Myo were high. At 14 days,these indices returned to normal gradually. The T2WI changes and T2 value were positively associated with the pathological changes of the muscles,serum sTnI and urine Myo changes. However,the signal intensity of T1WI did not vary significantly at different time points.
2. The serum levels of iFABP at 2,6,12h and 24h after injury in two groups of ischemic postconditioning were respectively IP-A : 108.75±4.81 , 117.04±3.70 ,125.52±4.22,109.12±6.95ng/ml and IP-B:108.62±3.05,117.83±3.45,127.93±3.86,106.59±3.92ng/ml.There was a significant descent compared with those in the control group. And also there was a significant descent in serum level of DAO at 2h and 6h after injury in two groups (I-post A:7.48±0.46,8.69±0.69U/ml,I-post B:7.43±0.46,8.70±0.70U/ml) compared with those in the control group(p<0.05).But there was no difference between the two groups of ischemic postconditioning. There was no difference in the pathological changes of ileum among all the group.
3. There was a significant descent in serum level of IL-6 and TNF-αat 2h,6h,12h and 24h after injury in two groups of ischemic postconditioning,and a significant increase in serum level of IL-10 at 2h,6h and 12h after injury in two groups to the control group(p<0.05).But there was no difference between the two groups of ischemic postconditioning(p>0.05).
Conclusions
1. T2WI and T2 value from T2 mapping are very useful methods of choice to evaluate the distribution and extension of the affected muscles. The high signal intensity on T2WI of the affected muscles after crush injury may be due to an increased extracellular space,local inflammation and incomplete muscle fiber regeneration.
2. Ischemic postconditioning can protect intestinal mucosa barrier on the model of hind limb crush injury in rabbits. The morphological restoration of intestinal mucosa is earlier than the function recovery of intestinal mucosa barrier.Ischemic postconditioning can inhibition SIRS on the model of hind limb crush injury in rabbits. This study shows that ischemic postconditioning may be a new way to treat limb crush injury.
引文
1. Guis S, Mattei JP, Cozzone PJ, et al. Pathophysiology and clinical presentations of rhabdomyolysis. Joint Bone Spine,2005,72(5):382–391.
2. Knochel JP. Mechanisms of rhabdomyolysis. Curr Opin Rheumatol,1993,5(6):725–731.
3. Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore),1982,61(3):141–152.
4. Campbell SE, Adler R, Sofka CM. Ultrasound of muscle abnormalities. Ultrasound Q 2005,21(2):87–94.
5. Lu CH, Tsang YM, Yu CW, et al. Rhabdomyolysis: magnetic resonance imaging and computed tomography findings. J Comput Assist Tomogr,2007,31(3):368-374.
6. Elsayes KM, Lammle M, Shariff A, et al. Value of magnetic resonance imaging in muscle trauma. Curr Probl Diagn Radiol,2006,35(5):206–212.
7. Trattnig S, Mamisch TC, Welsch GH, et al. Quantitative T2 mapping of matrix-associated autologous chondrocyte transplantation at 3 Tesla-an in vivo cross-sectional study. Invest Radiol,2007,42(6):442–448.
8. Blikslager AT, Roberts MC, Rhoads JM, et al. Is reperfusion injury an important cause of mucosal damage after porcine intestinal ischemia? Surgery,1997,121(5):526–534.
9. Afessa B, Green B, Delke I, et al.Systemic Inflammatory response syndrome,organ failure,and outcome in critically ill obstetric patients treated in an ICU.Chest,2001,120(4):1271-1277.
10. Torre D,Tambini R,Aristodemo S,et al.Anti-inflammatory response of IL 4,IL-10 and TGF-βin patients with systemic inflammatory response syndrome.Mediators Inflamm,2000,9(34):193-195.
11. Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic preconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol;2003,285(2):579-588.
12. Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res;2004, 62(1):74-85.
13. Yang XM, Proctor JB, Cui L, et al. Multiple, brief coronary occlusions during earlyreperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol; 2004, 44(5):1103-1110.
14. Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of“modified reperfusion”protects the myocardium by activating the phosphatidylinositol 3-kinase-Akt pathway. Circ Res;2004,95(3):230-232.
15. 15.I. Szwarc, S. Soullier, N. Gayrard,et al. Ischemic Postconditioning Prevents Ischemic Acute Renal Failure.Transplantation Proceedings;2007,39(8):2554–2556.
16. Fleckenstein JL, Weatherall PT, Bertocci LA, et al. Locomotor system assessment by muscle magnetic resonance imaging. Magn Reson Q,1991,7(2):79–103.
17. Stephan S,Johannes M, Arnold K,et al.Skeletal troponin I as a marker of exercise-induced muscle damage. J Appl Physiol,1997,83(4):1076-1082.
18. Jeremy A. Simpson, Ralf Labugger, Geoffrey G. Hesketh,et al. Differential Detection of Skeletal Troponin I Isoforms in Serum of a Patient with Rhabdomyolysis: Markers of Muscle Injury? Clinical Chemistry,2002,48(7):1112-1114.
19. Mosher, Timothy J,Dardzinski BJ. Cartilage MRI T2 Relaxation Time Mapping: Overview and Applications. Seminars in Musculoskeletal Radiology. Imaging in Arthritis,2004,8(4):355-368.
20. Astrid Watrin, Jean Pierre B. Ruaud, Pierre T. A. Olivier,et al. T2 Mapping of Rat Patellar Cartilage. Radiology,2001,219(2):395-402.
21. Chiu CJ,Mcardle AH,Brown R,et al.Intestinal mucosal lesion in low-flow states. I. A morphological, hemodynamic, and metabolic reappraisal.Arch Surg, 1970,101(4): 478– 483.
22. Szwarc, S. Soullier, N. Gayrard,et al. Ischemic Postconditioning Prevents Ischemic Acute Renal Failure.Transplantation Proceedings,2007,39(8):2554–2556.
23.石凤梧,蔡文清,陈子英,等.缺血后处理对猪心肌细胞Fas基因蛋白表达及Caspase-3活性的影响.中华实验外科杂志,2006,23(6):709-712.
24. Karin Przyklenk, Michelle Maynard, Chad E. Darling,et al.Aging Mouse Hearts Are efractory to Infarct Size Reduction With Post-Conditioning. J Am Coll Cardiol,2008,51(14):1393–1398.
25. M. Ozgur Taskapilioglu , Tulin Alkan, Bulent Goren,et al.Neuronal protective effects of focal ischemic pre- and/or postconditioning on the model of transient focal cerebralischemia in rats. Journal of Clinical Neuroscience,2009,16(5):693–697.
26. Bolli R, Patel BS, Jeroudi MO, et al.Demonstration of free radical generation in“stunned”myocardium of intact dogswith the use of the spin trap alpha-phenylN-tert-butylnitrone . J Clin Invest,1988,82(2):476-485.
27. Tsutsumi YM, Yokoyama T, Horikawa Y, et al.Reactive oxygen species trigger ischemic and pharmacologicalpostconditioning: in vivo and in vitro characterization. Life Sci,2007,81(15):1223-1227.
28.陶凌,李源,高峰,等.缺血后处理对急性心肌缺血再灌注兔心脏的保护作用.第四军医大学学报,2000,21(6):116-118.
29. Laskey WK. Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction: a pilot study.Catheter Cardiovasc Interv,2005,65(3):361-367.
30. Derin N,Izgut-Uysal VN,Agac A,et al. L-carnitine protects gastricmucosa by decreasing ischemia-reperfusion induced lipid peroxidation. J Physiol Pharmacol,2004,(3): 595-606.
31.褚薇薇,武步强,沙焕臣,等.缺血后处理对缺血-再灌注大鼠肠黏膜的抗损伤作用.西安交通大学学报:医学版,2007,28(2):149-151.
32.丁连安,黎介寿,李幼生,等.创伤及内毒素对大鼠肠屏障功能的损害.中华实验外科杂志,2004,21:697-699.
33.郑联合,马保安,孙宏慧等.急性脊髓损伤全身性炎症反应与ARDS及MODS.创伤外科杂志,2004,6(1):38-41.
34. Vincent Donckier, Patricia Loi, Jean Closset, et al. Preconditioning of donors with interleukin-10 reduces hepatic ischemia-reperfusion injury after liver transplantation in pigs. Transplantation,2003,75(6):902-904.
35. S.Salgar, E. Manning, S. Pham, et al. Interleukin-10 engineered mesenchymal stem cell therapy to prevent ischemia-reperfusion injury in lung transplants. Supplement to Transplantation,2008,86(2Supl.):58.
1. Gonzalez D. Crush syndrome. Critical Care Medicine,2005;33(1):34–41.
2. Fernandez WG, Hung O, Bruno R, et al. Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis. Am J Emerg Med,2005,23(1):1–7.
3. Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med,1990;322(7):825–829.
4.刘水平,刘小山,竞花兰等.挤压伤大鼠早期心脏损伤的细胞机制.法医学杂志,2006,22(2):90-92.
5. Kenan Keven, Kenan Ates, Mehmet Sukru Sever,et al. Infectious Complications after Mass Disasters:The Marmara Earthquake Experience. Scand J Infect Dis,2003,35(2): 110–113.
6. Trattnig S, Mamisch TC, Welsch GH, et al. Quantitative T2 mapping of matrix-associated autologous chondrocyte transplantation at 3 Tesla-an in vivo cross-sectional study. Invest Radiol,2007,42(6):442–448.
7. Ledermann HP, Heidecker HG, Schulte AC, et al. Calf muscles imaged at BOLD MR: correlation with TcPO2 and flowmetry measurements during ischemia and reactive hyperemia-initial experience. Radiology,2006,241(2):477–484.
8. Ledermann HP, Schulte AC, Heidecker HG, et al. Blood oxygenation level-dependent magnetic resonance imaging of the skeletal muscle in patients with peripheral arterial occlusive disease. Circulation,2006,113(25):2929–2935.
9. Stewart C. EMR textbook: Crush injuries. 2005.
10. Brown CV, Rhee P, Evans K, et al. Preventing renal failure in patients with rhabdomyolysis: Do bicarbonate and mannitol make a difference? J Trauma. 2004,56(6):1191–1196.
11. 11.I. Szwarc, S. Soullier, N. Gayrard,et al. Ischemic Postconditioning Prevents Ischemic Acute Renal Failure.Transplantation Proceedings,2007,39(8):2554–2556.
12.黄显凯,姚元章,王韬等.负压封闭引流在严重多发伤创面治疗中的作用.创伤外科杂志,2008,10(5):437-439.
13. Asenio JA, McDuffie L, Petrone P, Roldan′G, Forno W, Gambaro E, et al. Reliable variables in the exsanguinated patient which indicate damage control and predict outcome. Am J Surg, 2001,182(6):743–51.
14. S.S. Jaunoo, D.P. Harji. Damage control surgery. International Journal of Surgery ,2009,7(2):110–113.
15.熊雁,杜全印,孙红振等.损害控制救治平时和地震时严重多发伤的比较研究.中国骨伤,2008,21(10):726-728.
2. Knochel JP. Mechanisms of rhabdomyolysis. Curr Opin Rheumatol,1993,5(6):725–731.
3. Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore),1982,61(3):141–152.
4. Campbell SE, Adler R, Sofka CM. Ultrasound of muscle abnormalities. Ultrasound Q 2005,21(2):87–94.
5. Lu CH, Tsang YM, Yu CW, et al. Rhabdomyolysis: magnetic resonance imaging and computed tomography findings. J Comput Assist Tomogr,2007,31(3):368-374.
6. Elsayes KM, Lammle M, Shariff A, et al. Value of magnetic resonance imaging in muscle trauma. Curr Probl Diagn Radiol,2006,35(5):206–212.
7. Trattnig S, Mamisch TC, Welsch GH, et al. Quantitative T2 mapping of matrix-associated autologous chondrocyte transplantation at 3 Tesla-an in vivo cross-sectional study. Invest Radiol,2007,42(6):442–448.
8. Blikslager AT, Roberts MC, Rhoads JM, et al. Is reperfusion injury an important cause of mucosal damage after porcine intestinal ischemia? Surgery,1997,121(5):526–534.
9. Afessa B, Green B, Delke I, et al.Systemic Inflammatory response syndrome,organ failure,and outcome in critically ill obstetric patients treated in an ICU.Chest,2001,120(4):1271-1277.
10. Torre D,Tambini R,Aristodemo S,et al.Anti-inflammatory response of IL 4,IL-10 and TGF-βin patients with systemic inflammatory response syndrome.Mediators Inflamm,2000,9(34):193-195.
11. Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic preconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol;2003,285(2):579-588.
12. Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res;2004, 62(1):74-85.
13. Yang XM, Proctor JB, Cui L, et al. Multiple, brief coronary occlusions during earlyreperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol; 2004, 44(5):1103-1110.
14. Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of“modified reperfusion”protects the myocardium by activating the phosphatidylinositol 3-kinase-Akt pathway. Circ Res;2004,95(3):230-232.
15. 15.I. Szwarc, S. Soullier, N. Gayrard,et al. Ischemic Postconditioning Prevents Ischemic Acute Renal Failure.Transplantation Proceedings;2007,39(8):2554–2556.
16. Fleckenstein JL, Weatherall PT, Bertocci LA, et al. Locomotor system assessment by muscle magnetic resonance imaging. Magn Reson Q,1991,7(2):79–103.
17. Stephan S,Johannes M, Arnold K,et al.Skeletal troponin I as a marker of exercise-induced muscle damage. J Appl Physiol,1997,83(4):1076-1082.
18. Jeremy A. Simpson, Ralf Labugger, Geoffrey G. Hesketh,et al. Differential Detection of Skeletal Troponin I Isoforms in Serum of a Patient with Rhabdomyolysis: Markers of Muscle Injury? Clinical Chemistry,2002,48(7):1112-1114.
19. Mosher, Timothy J,Dardzinski BJ. Cartilage MRI T2 Relaxation Time Mapping: Overview and Applications. Seminars in Musculoskeletal Radiology. Imaging in Arthritis,2004,8(4):355-368.
20. Astrid Watrin, Jean Pierre B. Ruaud, Pierre T. A. Olivier,et al. T2 Mapping of Rat Patellar Cartilage. Radiology,2001,219(2):395-402.
21. Chiu CJ,Mcardle AH,Brown R,et al.Intestinal mucosal lesion in low-flow states. I. A morphological, hemodynamic, and metabolic reappraisal.Arch Surg, 1970,101(4): 478– 483.
22. Szwarc, S. Soullier, N. Gayrard,et al. Ischemic Postconditioning Prevents Ischemic Acute Renal Failure.Transplantation Proceedings,2007,39(8):2554–2556.
23.石凤梧,蔡文清,陈子英,等.缺血后处理对猪心肌细胞Fas基因蛋白表达及Caspase-3活性的影响.中华实验外科杂志,2006,23(6):709-712.
24. Karin Przyklenk, Michelle Maynard, Chad E. Darling,et al.Aging Mouse Hearts Are efractory to Infarct Size Reduction With Post-Conditioning. J Am Coll Cardiol,2008,51(14):1393–1398.
25. M. Ozgur Taskapilioglu , Tulin Alkan, Bulent Goren,et al.Neuronal protective effects of focal ischemic pre- and/or postconditioning on the model of transient focal cerebralischemia in rats. Journal of Clinical Neuroscience,2009,16(5):693–697.
26. Bolli R, Patel BS, Jeroudi MO, et al.Demonstration of free radical generation in“stunned”myocardium of intact dogswith the use of the spin trap alpha-phenylN-tert-butylnitrone . J Clin Invest,1988,82(2):476-485.
27. Tsutsumi YM, Yokoyama T, Horikawa Y, et al.Reactive oxygen species trigger ischemic and pharmacologicalpostconditioning: in vivo and in vitro characterization. Life Sci,2007,81(15):1223-1227.
28.陶凌,李源,高峰,等.缺血后处理对急性心肌缺血再灌注兔心脏的保护作用.第四军医大学学报,2000,21(6):116-118.
29. Laskey WK. Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction: a pilot study.Catheter Cardiovasc Interv,2005,65(3):361-367.
30. Derin N,Izgut-Uysal VN,Agac A,et al. L-carnitine protects gastricmucosa by decreasing ischemia-reperfusion induced lipid peroxidation. J Physiol Pharmacol,2004,(3): 595-606.
31.褚薇薇,武步强,沙焕臣,等.缺血后处理对缺血-再灌注大鼠肠黏膜的抗损伤作用.西安交通大学学报:医学版,2007,28(2):149-151.
32.丁连安,黎介寿,李幼生,等.创伤及内毒素对大鼠肠屏障功能的损害.中华实验外科杂志,2004,21:697-699.
33.郑联合,马保安,孙宏慧等.急性脊髓损伤全身性炎症反应与ARDS及MODS.创伤外科杂志,2004,6(1):38-41.
34. Vincent Donckier, Patricia Loi, Jean Closset, et al. Preconditioning of donors with interleukin-10 reduces hepatic ischemia-reperfusion injury after liver transplantation in pigs. Transplantation,2003,75(6):902-904.
35. S.Salgar, E. Manning, S. Pham, et al. Interleukin-10 engineered mesenchymal stem cell therapy to prevent ischemia-reperfusion injury in lung transplants. Supplement to Transplantation,2008,86(2Supl.):58.
1. Gonzalez D. Crush syndrome. Critical Care Medicine,2005;33(1):34–41.
2. Fernandez WG, Hung O, Bruno R, et al. Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis. Am J Emerg Med,2005,23(1):1–7.
3. Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med,1990;322(7):825–829.
4.刘水平,刘小山,竞花兰等.挤压伤大鼠早期心脏损伤的细胞机制.法医学杂志,2006,22(2):90-92.
5. Kenan Keven, Kenan Ates, Mehmet Sukru Sever,et al. Infectious Complications after Mass Disasters:The Marmara Earthquake Experience. Scand J Infect Dis,2003,35(2): 110–113.
6. Trattnig S, Mamisch TC, Welsch GH, et al. Quantitative T2 mapping of matrix-associated autologous chondrocyte transplantation at 3 Tesla-an in vivo cross-sectional study. Invest Radiol,2007,42(6):442–448.
7. Ledermann HP, Heidecker HG, Schulte AC, et al. Calf muscles imaged at BOLD MR: correlation with TcPO2 and flowmetry measurements during ischemia and reactive hyperemia-initial experience. Radiology,2006,241(2):477–484.
8. Ledermann HP, Schulte AC, Heidecker HG, et al. Blood oxygenation level-dependent magnetic resonance imaging of the skeletal muscle in patients with peripheral arterial occlusive disease. Circulation,2006,113(25):2929–2935.
9. Stewart C. EMR textbook: Crush injuries. 2005.
10. Brown CV, Rhee P, Evans K, et al. Preventing renal failure in patients with rhabdomyolysis: Do bicarbonate and mannitol make a difference? J Trauma. 2004,56(6):1191–1196.
11. 11.I. Szwarc, S. Soullier, N. Gayrard,et al. Ischemic Postconditioning Prevents Ischemic Acute Renal Failure.Transplantation Proceedings,2007,39(8):2554–2556.
12.黄显凯,姚元章,王韬等.负压封闭引流在严重多发伤创面治疗中的作用.创伤外科杂志,2008,10(5):437-439.
13. Asenio JA, McDuffie L, Petrone P, Roldan′G, Forno W, Gambaro E, et al. Reliable variables in the exsanguinated patient which indicate damage control and predict outcome. Am J Surg, 2001,182(6):743–51.
14. S.S. Jaunoo, D.P. Harji. Damage control surgery. International Journal of Surgery ,2009,7(2):110–113.
15.熊雁,杜全印,孙红振等.损害控制救治平时和地震时严重多发伤的比较研究.中国骨伤,2008,21(10):726-728.