Peng Na, Xiang Ding-Cheng, Su Lei
Department of Intensive Care Unit, Guangzhou General Hospital of Guangzhou Command, Guangzhou 510010, Guangdong, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Jun;22(6):364-6.
To investigate the myocardial protective effects of different dosage of ulinastatin (UTI) and the possible mechanism in septic rats.
Forty male Sprague-Dawley (SD) rats were randomly divided into five groups: control group, sham group, model group, UTI in low dose or high dose group. Cecal ligation and puncture (CLP) was adopted to reproduce animal model of sepsis. Left ventricular myocardium was harvested and blood samples were collected at 24 hours after successful establishment of animal model. Serum cardiac troponin I (cTnI), the contents of myocardial tumor necrosis factor-alpha (TNF-alpha) and endothelin-1 (ET-1) were measured, and myocardial pathological changes were observed.
In the model group, the level of serum cTnI, and the expressions of myocardial TNF-alpha and ET-1 were much higher than those in control group [cTnI (microg/L): 7.58+/-0.53 vs. 1.05+/-0.21, TNF-alpha (pg/g): 945.6+/-72.0 vs. 238.2+/-35.2, ET-1 (pg/g): 776.8+/-123.9 vs. 170.1+/-28.3, all P<0.01]. There were no differences in the levels of serum cTnI, myocardial TNF-alpha and ET-1 between low dose UTI group and the model group [cTnI (microg/L): 7.21+/-0.51 vs. 7.58+/-0.53, TNF-alpha (pg/g): 910.5+/-96.6 vs. 945.6+/-72.0, ET-1 (pg/g): 714.0+/-66.7 vs. 776.8+/-123.9, all P>0.05]. However, serum cTnI, myocardial TNF-alpha and ET-1 were lower significantly in high dose UTI group than in model group [cTnI (microg/L): 4.30+/-0.84 vs. 7.58+/-0.53, TNF-alpha (pg/g): 430.5+/-75.6 vs. 945.6+/-72.0, ET-1 (pg/g): 377.1+/-39.0 vs. 776.8+/-123.9, all P<0.01].
High dose (but not low dose) UTI may protect myocardium from the damage resulted from sepsis in a rat model, probably by lowering expressions of TNF-alpha and ET-1.
探讨不同剂量乌司他丁（UTI）对脓毒症大鼠的心肌保护作用及其可能机制。
40只雄性Sprague-Dawley（SD）大鼠随机分为五组：对照组、假手术组、模型组、低剂量UTI组和高剂量UTI组。采用盲肠结扎穿孔术（CLP）制备脓毒症动物模型。成功建立动物模型后24小时，采集左心室心肌组织并收集血样。检测血清心肌肌钙蛋白I（cTnI）、心肌肿瘤坏死因子-α（TNF-α）和内皮素-1（ET-1）含量，并观察心肌病理变化。
模型组血清cTnI水平、心肌TNF-α和ET-1表达均显著高于对照组[cTnI（μg/L）：7.58±0.53 vs. 1.05±0.21，TNF-α（pg/g）：945.6±72.0 vs. 238.2±35.2，ET-1（pg/g）：776.8±123.9 vs. 170.1±28.3，均P<0.01]。低剂量UTI组血清cTnI水平、心肌TNF-α和ET-1与模型组比较，差异无统计学意义[cTnI（μg/L）：7.21±0.51 vs. 7.58±0.53，TNF-α（pg/g）：910.5±96.6 vs. 945.6±72.0，ET-1（pg/g）：714.0±66.7 vs. 776.8±123.9，均P>0.05]。高剂量UTI组血清cTnI水平、心肌TNF-α和ET-1显著低于模型组[cTnI（μg/L）：4.30±0.84 vs. 7.58±0.53，TNF-α（pg/g）：430.5±75.6 vs. 945.6±72.0，ET-1（pg/g）：377.1±39.0 vs. 776.8±123.9，均P<0.01]。
高剂量（而非低剂量）UTI可能通过降低TNF-α和ET-1表达，保护脓毒症大鼠模型的心肌免受损伤。
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