[Effect of acupuncture on diaphragmatic function in patients with AECOPD typeâ ¡ respiratory failure evaluated by ultrasound detection].

OBJECTIVE: To observe the therapeutic effect of acupuncture combined with western conventional therapy on type Ⅱ respiratory failure of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and evaluate the effect of acupuncture on diaphragmatic function and prognosis by bedside ultrasound. METHODS: A total of 111 patients with AECOPD type Ⅱ respiratory failure were randomized into an acupuncture group, a conventional treatment group and a non-acupoint acupuncture group, 37 cases in each one. The routine AECOPD nursing care and treatment with western medicine were provided in the 3 groups. Additionally, in the acupuncture group, acupuncture was applied at Dingchuan (EX-B 1), Feishu (BL 13), Taiyuan (LU 9), Danzhong (CV 17) and Zhongwan (CV 12), etc. In the non-acupoint acupuncture group, acupuncture was given at the points 5 to 10 mm lateral to each of the acupoints selected in the acupuncture group. Acupuncture was given once every day, 30 min each time, consecutively for 10 days in the above two groups. Separately, before treatment, on day 3, 7 and 10 of treatment, arterial partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2) and diaphragm thickening fraction (TFdi) were observed in each group. Before and after treatment, the inflammatory and immune indexes (levels of white blood cell [WBC], procalcitonin [PCT], hypersensitive C-reactive protein [hs-CRP] and T lymphocyte percentage [ %]), auxiliary respiratory muscle movement score, the score of chronic obstructive pulmonary disease (COPD) assessment test (CAT), the score of the modified British Medical Research Council dyspnea scale (mMRC) and the TCM syndrome score were compared in each group. The duration of mechanical ventilation, relative complications, 14-day clinical controlled discharge rate and the therapeutic effect were observed in each group. RESULTS: On day 3, 7 and 10 of treatment, PaO2 and TFdi were all increased as compared with those before treatment (P<0.01) and PaCO2 was reduced as compared with that before treatment in each group (P<0.01). After treatment, % was increased as compared with that before treatment in each group (P<0.01), WBC, PCT, hs-CRP, auxiliary respiratory muscle movement score, CAT score, mMRC score and TCM syndrome score were all reduced as compared with those before treatment in each group (P<0.01). After treatment, PaCO2, WBC, PCT, hs-CRP, auxiliary respiratory muscle movement score, CAT score and mMRC score in the acupuncture group were all lower than the other two groups (P<0.01), PaO2 and TFdi were higher than the other two groups (P<0.01); % was higher and TCM syndrome score was lower in the acupuncture group compared with those in the non-acupoint acupuncture group (P<0.01). The duration of mechanical ventilation and the total incidence of complications in the acupuncture group were all lower than the other two groups (P<0.01), and the 14-day clinical controlled discharge rate and total clinical effective rate were higher than the other two groups (P<0.01). CONCLUSION: Acupuncture as adjunctive therapy achieves significant therapeutic effect on AECOPD type Ⅱ respiratory failure. It improves diaphragmatic function, promotes oxygenation and relieves carbon dioxide retention of artery, alleviates clinical symptoms and reduces the time of mechanic ventilation and hospitalization. Besides, the bedside ultrasound detection can objectively reflect the effect of acupuncture on diaphragmatic function in the patients with AECOPD complicated with typeⅡrespiratory failure.

Shenfu injection attenuates lipopolysaccharide-induced myocardial inflammation and apoptosis in rats.

Shenfu injection (SFI), a Chinese medicinal product, shows potent efficacy in treating sepsis. The aim of the present study was to clarify the protective effects of SFI against lipopolysaccharide (LPS)-induced myocardial inflammation and apoptosis. Experiments were carried out in Sprague-Dawley (SD) rats treated with LPS or LPS + SFI, and in H9C2 cardiomyocytes. The sepsis-associated myocardial inflammation and apoptosis was induced by the intraperitoneal injection of LPS (20 mg·kg-1). SFI attenuated the increased expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß induced by LPS both in serum and heart. In LPS group, cell viability was reduced, and reversed after SFI administration. LPS treatment increased the expression levels of cleaved-caspase 3 and Bax, and those of Bcl2 and Bcl2/Bax. These two trends were reversed by SFI administration. The expression levels of phosphorylated mitogen-activated protein kinase kinase (p-MEK) and phosphorylated extracellular regulated protein kinases (p-ERK) were increased by LPS, and reversed by SFI. MEK inhibitor U0126 attenuated the apoptosis induced by LPS. These results indicate that SFI could treat LPS-induced cardiac dysfunction. In conclusion, SFI attenuates the inflammation and apoptosis induced by LPS via downregulating the MEK and ERK signaling pathways.