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目的在观察10%缺氧复合缺水缺食对心脏结构和功能影响的基础上,探讨Ca2+信号转导相关因子在其中的作用。方法将80只Wistar大鼠随机分为对照组、缺氧组、缺食缺水组和缺氧缺食缺水组[置于常压低氧舱(10%氧浓度)并禁食水],于第1、3、5、7天,采用全自动血生化仪检测血清代谢酶改变,透射电镜观察心脏超微结构改变,采用免疫组化检测心肌钙调素和磷酸化环磷酸腺苷反应元件结合蛋白(CREB)表达变化。结果 10%缺氧缺水缺食后7 d,大鼠血清乳酸脱氢酶[(1628.40±460.8)U/L]和谷草转氨酶[(394.60±187.18)U/L]活性明显高于对照组[分别为(578.40±135.04)、(136.40±14.59)U/L];心肌细胞核型不整,染色质边集,核周间隙增宽,线粒体肿胀空化或代偿性增加、Z线紊乱甚至溶解,肌浆网轻度扩张;心肌肌膜肿胀,呈指状突起;间质细胞和血管内皮细胞退变或凋亡;心肌细胞胞浆钙调素(4.22±0.84)与心肌细胞核磷酸化CREB表达(3.57±0.55)明显高于对照组[分别为(0.73±0.41)、(0.90±0.41)]。结论 10%缺氧复合缺水缺食可引起大鼠心脏结构和功能损伤,其机制可能与Ca2+信号通路激活(钙调素和磷酸化CREB表达增加)有关。
Objective To observe the effects of 10% hypoxia combined with water deficit on cardiac structure and function, and to explore the role of Ca2 + signal transduction related factors. Methods Eighty Wistar rats were randomly divided into control group, hypoxia group, lack of water group and hypoxic-ischemic group [placed in normobaric hypoxia chamber (10% oxygen concentration) and fasting water] On the 1st, 3rd, 5th and 7th days, the serum metabolic enzymes were detected by automatic blood biochemical analyzer. The changes of cardiac ultrastructure were observed by transmission electron microscopy. The expressions of cardiac calmodulin and phosphorylated cyclic adenosine monophosphate Binding protein (CREB) expression changes. Results Serum levels of lactate dehydrogenase [(1628.40 ± 460.8) U / L] and aspartate aminotransferase [(394.60 ± 187.18) U / L] were significantly higher than those of the control group on the 7th day after hypoxia / (578.40 ± 135.04) and (136.40 ± 14.59) U / L, respectively. The karyotypes of cardiomyocytes were irregular, the chromatin marginal zone was broadened, the perinuclear space was broadened, the mitochondria were swollen and cavitated or compensated, the Z line was disturbed or even dissolved, Sarcoplasmic reticulum mild dilatation; myocardial muscle membrane swelling, finger-like protrusions; interstitial cells and vascular endothelial cell degeneration or apoptosis; cardiomyocyte cytoplasmic calmodulin (4.22 ± 0.84) and myocardial cell nuclear phosphorylated CREB expression 3.57 ± 0.55) was significantly higher than that of the control group [(0.73 ± 0.41) and (0.90 ± 0.41)] respectively. Conclusions 10% hypoxia combined with water deficit can cause cardiac structural and functional injury in rats. The mechanism may be related to the activation of Ca2 + signaling pathway (increased expression of calmodulin and phosphorylated CREB).