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

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.