| ObjectiveRhabdomyolysis 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.Methods1. 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.Results1. 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).Conclusions1. 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.
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