机构地区:[1]云南省第一人民医院急诊ICU,云南昆明650032
出 处:《昆明医科大学学报》2013年第2期27-31,共5页Journal of Kunming Medical University
摘 要:目的探讨米力农注射液对脓毒症大鼠心肌损伤的保护作用及其可能机制.方法 SD雄性大鼠45只,按随机数字分为对照组、假手术组、模型组及米力农小剂量组、大剂量组.采用盲肠结扎穿孔术(CLP)建立脓毒症模型,24 h后取动脉血及左室心肌,检测血清心肌肌钙蛋白I(cTn)I、心肌同工酶CK-MB,心肌组织匀浆上清液肿瘤坏死因子-α(TNF-α)、核因子κB(NF-κB)及内皮素-1(ET-1)水平,观察心肌组织病理学改变.结果模型组血清cTnI、CK-MB及心肌TNF-α、ET-1、NF-κB水平较正常对照组明显升高;[cTnI(μg/L)]:(19.425±0.637)比(1.015±0.210);[CK-MB(μg/L)]:(4970.50±562.56)比(423.67±21.92);[TNF-α(pg/L)]:(956.70±72.61)比(239.63±37.21),[ET-1(pg/L)]:(786.92±126.30)比(175.12±28.35),[NF-kB(μg/mL)]:(53.96±11.29)比(11.84±2.95);均P<0.01.米力农小剂量组血清cTnI,CK-MB及TNF-α,ET-I、NF-kB水平与模型组比较差异无统计学意义;[cTnI(ug/L)]:(15.572±0.398)比(19.425±0.637);[CK-MB(μg/L)]:(4698.52±501.52)比(4970.50±562.56);[TNF-α(pg/L)]:(912.50±96.67)比(956.70±72.61);[ET-1(pg/L)]:(716.52±63.71)比(786.92±126.30),[NF-kB(μg/mL)]:(47.39±12.35)比(53.96±11.29);均P>0.05.米力农大剂量组血清cTnI、CK-MB及心肌TNF-α、ET-1、NF-kB较模型组明显降低,[cTnI(μg/L)]:(3.520±0.267)比(19.425±0.637);[CK-MB(μg/L)]:(3920.00±516.49)比(4 970.50±562.56);[TNF-α(pg/L)]:(442.53±75.67)比(956.70±72.61);[ET-1(pg/L)]:(279.42±37.59)比(786.92±126.30),[NF-κB(μg/mL)]:(21.18±8.19)比(53.96±11.29);均P<0.01.结论大剂量米力农对脓毒症心肌损伤具有保护作用,其机制可能通过抑制心肌TNF-α、ET-1、NF-κB的表达而实现;小剂量米力农对脓毒症心肌损伤无保护作用.Objective To investigate the protective effect and mechanism of Milrinone injection on the myocardial damage in rats with sepsis. Methods 45 male SD rats were randomly divided into 5 groups: control group, sham operation group, model group and low-dose milrinone group and high-dose group. The sepsis models were established by cecal ligation and puncture (CLP) . Serum levels of cardiac troponin I (cTnI), cardiac enzyme CK-MB and myocardial tissue homogenate tumor necrosis factor-a (TNF-α) , nuclear factor-k-gene binding (NF- s: B) and endothelin -1 (ET-1) levels were detected in the artery blood after 24 hours. We also observed the histopathological changes of left ventricular myocardia. Results The serum levels of cTnI and CK-MB and the myocardial levels of TNF-α , NF- s: B and ET-1 in the model group were significantly higher than the normal eontrolgroup. ~eTnI (ug/L) 3: (19.425+0.637) vs (1.015±0.210); ECK-MB (ug/L)~ : (4970.50± 562.56) vs ( 423.67 ±21.92) ; ETNF-a (pg/L) ~ : (956.70 ~72.61) vs (239.63 ±37.21) , ET-1 (pg/L) : (786.92±126.30) vs (175.12±28.35), ~NF-KB (ug/ml) 3 : (53.96±11.29) vs (11.84± 2.95) ; P〈O.01. The serum levels of cTnI and CK-MB and the myocardial levels ofTNF-a , NF- K B and ET-1 had no statistically significant differences between model group and low-dose milrinone group. I cTnI (ug/L) : (15.572±0.398) vs (19.425±0.637), CK-MB (ug/L)~ : (4698.52±501.52) vs (4970.50±562.56); ETNF-a (pg/L) l : (912.50±96.67) vs (956.70±72.61); ~ET-1 (pg/L)~ : (716.52±63.71) vs (786.92 ± 126.30) , NF- K B (ug/ml) : (47.39 ± 12.35) vs (53.96 + 11.29) (P:〉O.05) . The serum levels of cTnI and CK-MB and the myocardial levels ofTNF-α , NF- K B and ET-1 in the high-dose group were significantly lower than the model group. IcTnI (ug/L)α~ : (3.520 ± 0.267) vs (19.425 ± 0.637) ; CK-MB (ug/L) �
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