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首页> 外文期刊>Medecine et maladies infectieuses >Caecal infestation due to Enterobius vermicularis [Atteinte c?cale à Enterobius vermicularis]
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Caecal infestation due to Enterobius vermicularis [Atteinte c?cale à Enterobius vermicularis]

机译:肠球菌引起的盲肠感染[Atteinte c?caleàEnterobius vermicularis]

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Metabolic syndrome is known to increase the risk of abnormal cardiac structure and function, which are considered to contribute to increased incidence of cardiovascular disease and mortality. We previously demonstrated that ventricular hypertrophy and diastolic dysfunction occur in SHRSP.Z-Leprfa/IzmDmcr (SHRSP fatty) rats with metabolic syndrome. The aim of this study was to investigate the possible mechanisms underlying abnormal heart function in SHRSP fatty rats. The amount of sarcoplasmic reticulum Ca2+-ATPase (SERCA) 2a, phospholamban (PLB) protein, and Ser16-phosphorylated PLB was decreased in cardiomyocytes from SHRSP fatty rats compared with those from control Wistar-Kyoto rats at 18 weeks of age, and the PLB-to-SERCa2+a ratio was increased. Left ventricular developed pressure was unchanged, and coronary flow rate and maximum rate of left ventricular pressure decline (-dP/dt) was decreased in SHRSP fatty rats. Treatment with telmisartan reversed the abnormalities of PLB amount, coronary flow rate, and -dP/dt in SHRSP fatty rats. These results indicate that abnormal amounts of intracellular Ca2+ regulatory proteins in cardiomyocytes, leading to reduced intracellular Ca2+ reuptake into the sarcoplasmic reticulum, may play a role in the diastolic dysfunction in SHRSP fatty rats and that these effects are partially related to decreased coronary circulation. Telmisartan may be beneficial in protecting against disturbances in cardiac function associated with metabolic syndrome.
机译:已知代谢综合征会增加心脏结构和功能异常的风险,这被认为会增加心血管疾病的发生率和死亡率。我们先前证明,SHRSP.Z-Leprfa / IzmDmcr(SHRSP脂肪)大鼠患有代谢综合征时会发生心室肥大和舒张功能障碍。这项研究的目的是调查SHRSP脂肪大鼠心脏功能异常的潜在机制。与18周龄的Wistar-Kyoto对照大鼠和PLB相比,SHRSP脂肪大鼠心肌细胞的肌浆网C​​a2 + -ATPase(SERCA)2a,磷酸lamban(PLB)蛋白和Ser16磷酸化PLB减少-SERCa2 + a比增加。 SHRSP脂肪大鼠的左心室发育压力未改变,冠状动脉流速和左心室最大压力下降率(-dP / dt)降低。替米沙坦治疗可逆转SHRSP脂肪大鼠的PLB量,冠状动脉流速和-dP / dt异常。这些结果表明,心肌细胞中异常数量的胞内Ca2 +调节蛋白导致减少的胞内Ca2 +重吸收进入肌质网,可能在SHRSP脂肪大鼠的舒张功能障碍中起作用,并且这些作用部分与冠状动脉循环减少有关。替米沙坦可能有益于预防与代谢综合征相关的心脏功能障碍。

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