Risk factors affecting postoperative pulmonary function in congenital diaphragmatic hernia

Purpose@#It is well known that congenital diaphragmatic hernia (CDH) in infants impacts pulmonary function rehabilitation after surgery. However, the risk factors of postoperative pulmonary function are still unclear. In this research, we analyzed the potential risk factors of postoperative pulmonary function in CDH patients in order to improve the clinical management of CDH patients. @*Methods@#Thirty-three cases CDH infants followed were enrolled from November 2016 to September 2018. Clinical data were reviewed. Tidal breathing pulmonary function testing was performed after surgery. Correlation between pulmonary function and clinical characteristics was evaluated using multivariate analysis of variance. @*Results@#Pulmonary dysfunction was detected in 87.9% patients (29 of 33). The defect size was found to be significantly larger in patients with obstructed and mixed ventilatory disorders (P = 0.001). Diagnosis of gestational age (GA) was also significantly earlier compared to restrictive ventilatory disorders (P = 0.001). Larger defect size, and earlier prenatal diagnosis of GA were detected in severe obstructive ventilatory disorders (P = 0.007, P = 0.001, retrospectively). @*Conclusion@#Most patients had various degrees of pulmonary dysfunction after surgery. Patients with larger defect size and earlier diagnosis time might be vulnerable to severe obstructive and mixed ventilatory disorders.

Colonic Dysmotility in Murine Partial Colonic Obstruction Due to Functional Changes in Interstitial Cells

BACKGROUND/AIMS: Interstitial cells play important roles in gastrointestinal (GI) neuro-smooth muscle transmission. The underlying mechanisms of colonic dysmotility have not been well illustrated. We established a partial colon obstruction (PCO) mouse model to investigate the changes of interstitial cells and the correlation with colonic motility. METHODS: Western blot technique was employed to observe the protein expressions of Kit, platelet-derived growth factor receptor-α (Pdgfra), Ca²⁺-activated Cl⁻ (Ano1) channels, and small conductance Ca²⁺- activated K⁺ (SK) channels. Colonic migrating motor complexes (CMMCs) and isometric force measurements were employed in control mice and PCO mice. RESULTS: PCO mice showed distended abdomen and feces excretion was significantly reduced. Anatomically, the colon above the obstructive silicone ring was obviously dilated. Kit and Ano1 proteins in the colonic smooth muscle layer of the PCO colons were significantly decreased, while the expression of Pdgfra and SK3 proteins were significantly increased. The effects of a nitric oxide synthase inhibitor (L-NAME) and an Ano1 channel inhibitor (NPPB) on CMMC and colonic spontaneous contractions were decreased in the proximal and distal colons of PCO mice. The SK agonist, CyPPA and antagonist, apamin in PCO mice showed more effect to the CMMCs and colonic smooth muscle contractions. CONCLUSIONS: Colonic transit disorder may be due to the downregulation of the Kit and Ano1 channels and the upregulation of SK3 channels in platelet-derived growth factor receptor-α positive (PDGFRα⁺) cells. The imbalance between interstitial cells of Cajal-Ano1 and PDGFRα-SK3 distribution might be a potential reason for the colonic dysmotility.

Colonic Transit Disorder Mediated by Downregulation of Interstitial Cells of Cajal/Anoctamin-1 in Dextran Sodium Sulfate-induced Colitis Mice

BACKGROUND/AIMS: Interstitial cells of Cajal (ICC) and their special calcium-activated chloride channel, anoctamin-1 (ANO1) play pivotal roles in regulating colonic transit. This study is designed to investigate the role of ICC and the ANO1 channel in colonic transit disorder in dextran sodium sulfate (DSS)-treated colitis mice. METHODS: Colonic transit experiment, colonic migrating motor complexes (CMMCs), smooth muscle spontaneous contractile experiments, intracellular electrical recordings, western blotting analysis, and quantitative polymerase chain reaction were applied in this study. RESULTS: The mRNA and protein expressions of c-KIT and ANO1 channels were significantly decreased in the colons of DSS-colitis mice. The colonic artificial fecal-pellet transit experiment in vitro was significantly delayed in DSS-colitis mice. The CMMCs and smooth muscle spontaneous contractions were significantly decreased by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), an ANO1 channel blocker, and NG-Nitro-L-arginine methyl ester hydrochloride (L-NAME), an inhibitor of nitric oxide synthase activity, in DSS-colitis mice compared with that of control mice. Intracellular electrical recordings showed that the amplitude of NPPB-induced hyperpolarization was more positive in DSS-colitis mice. The electric field stimulation-elicited nitric-dependent slow inhibitory junctional potentials were also more positive in DSS-colitis mice than those of control mice. CONCLUSION: The results suggest that colonic transit disorder is mediated via downregulation of the nitric oxide/ICC/ANO1 signalling pathway in DSS-colitis mice.

Effect of Shenshuai Capsule on renal function, NO and TNF-? in blood of rats with chronic renal failure / 中成药

AIM: To explore the effect of Shenshuai Capsule on renal functio n, NO and TNF-? in CRF rat's blood. METHODS: Wister rats were fed with adenine to establish the chronic renal insufficiency anemia model, and then they were divided into three groups and fed with Shenshuai Capsule (high or low dosage) and Niaoduqing proup, respec tively. Kidney function index and the levels of NO and TNF-? in blood of CR F rats were measured. RESULTS: The comparison of renal function between the treatment gro up (high dosage) and the Niaoduqing group were significantly different respectiv ely. At the same time, Shenshuai Capsule can increase the NO of CRF rat's blood and reduce the TNF-?. CONCLUSION: Shenshuai Capsule can improve renal function of CRF rat , simultaneously raise the NO of CRF rat's blood and reduce the TNF-?. The lat ter may be one of the mechanism of action that Shunshuai Capsule can delay the r enal failure.