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Diaphragmatic dysfunction in sepsis due to severe acute pancreatitis complicated by intra-abdominal hypertension

机译:重症急性胰腺炎并发腹内高压导致败血症的肌功能障碍

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Objective This study aimed to examine the mechanism of diaphragmatic dysfunction in sepsis due to severe acute pancreatitis (SAP) with intra-abdominal hypertension (IAH) in a rat model. Methods The rats were assigned at random to four groups: (1) control (n?=?5), (2) SAP (n?=?5), (3) SAP+IAH (n?=?5), and (4) SAP+IAH+SS-31 (n?=?5). Length and force output of the diaphragm were analysed in vivo . Histopathological examinations were performed by haematoxylin–eosin. Oxidative stress levels related to protease in diaphragmatic mitochondria were detected with a colorimetric technique. Results In the septic rat model due to SAP complicated by IAH, myofibres were increased. Muscle contractile function was significantly lower in the SAP+IAH group compared with the SAP and control groups. Glutathione peroxidase and superoxide dismutase levels were significantly lower and malondialdehyde levels were higher in the SAP and SAP+IAH groups compared with the control group. Notably, SS-31 could reverse atrophy of myofibres in SAP+IAH rats, as well as contractile dysfunction and mitochondrial dysfunction in the diaphragm. Conclusions Diaphragmatic structure and biomechanics are altered in septic rats due to SAP and IAH. This finding is mainly due to an increase in release of mitochondrial reactive oxygen species.
机译:目的探讨大鼠重症急性胰腺炎(SAP)合并腹内高压(IAH)引起的脓毒症的diaphragm肌功能障碍的机制。方法将大鼠随机分为四组:(1)对照(n?=?5),(2)SAP(n?=?5),(3)SAP + IAH(n?=?5)和(4)SAP + IAH + SS-31(n≥5)。膜片的长度和力输出进行了体内分析。组织病理学检查由苏木精-曙红进行。用比色法检测diaphragm肌线粒体中与蛋白酶相关的氧化应激水平。结果在SAP合并IAH引起的败血症大鼠模型中,肌纤维增加。与SAP和对照组相比,SAP + IAH组的肌肉收缩功能明显降低。与对照组相比,SAP和SAP + IAH组的谷胱甘肽过氧化物酶和超氧化物歧化酶水平显着降低,丙二醛水平更高。值得注意的是,SS-31可以逆转SAP + IAH大鼠的肌纤维萎缩,以及diaphragm肌的收缩功能障碍和线粒体功能障碍。结论SAP和IAH可导致脓毒症大鼠Dia肌结构和生物力学发生改变。该发现主要是由于线粒体活性氧的释放增加。

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