Adjuvant Therapy: YiqiDitanTongfu Decoction With External Diaphragm Pacer for Chronic Obstructive Pulmonary Disease Patients With Difficulty Weaning From Mechanical Ventilation.

CONTEXT: Global morbidity from chronic obstructive pulmonary disease (COPD) is high worldwide. Diaphragm pacing (DP) can maintain the natural, negative pressure breathing of COPD patients with diaphragmatic muscle dysfunction. The YiqiDitanTongfu (YDTF) decoction has been used clinically with COPD patients to help them to wean from mechanical ventilation, with their ventilation functions being improved and the success rate of weaning being largely increased. OBJECTIVE: The study intended to investigate the combined therapeutic effects of external DP and the YDTF decoction for COPD patients who have had difficulty weaning from mechanical ventilation. DESIGN: This study was a retrospective cohort study. SETTING: The study occurred at the Hebei General Hospital and Hebei Province Chest Hospital (Hebei Province, Shijiazhuang, China). PARTICIPANTS: Participants were 90 patients with COPD + type 1 respiratory failure, 101 patients with COPD + Type 2 respiratory failure, and 96 patients with COPD at the compensated stage. INTERVENTION: The participants were randomly divided into 3 groups: (1) traditional treatment (control group), (2) traditional treatment plus treatment with a diaphragm pacemaker (DP group), and (3) traditional treatment plus treatment with a DP and a YDTF decoction (DP + YDTF group). All treatments occurred for 12 d. OUTCOME MEASURES: Relevant outcomes were measured and compared at baseline and postintervention, including the rapid shallow breathing index, tidal volume, maximum inspiratory pressure, degree of diaphragmatic muscle activity, maximum expiratory pressure, the successful rates of weaning from mechanical ventilation, the potential of hydrogen, the partial pressure of oxygen, partial pressure of carbon dioxide, and oxygen saturation. RESULTS: The patients treated with the DP plus the YDTF decoction were more successful in weaning from mechanical ventilation than those treated with DP. Of the patients with COPD + type 1 respiratory failure, 86.67% succeeded vs 70.00% of the DP patients. Of patients with COPD + type 2 respiratory failure, 87.88% succeeded vs 79.41% of the DP patients. CONCLUSION: The DP plus the YDTF concoction acted as a successful treatment for heart failure caused by CPOD in comparison with the DP or YDTF alone, providing evidence that the DP + YDTF concoction can serve as a competitive method for helping COPD patients to wean from mechanical ventilation.

[Effects of hydrogen sulfide on mitochondria of lung in rats with ALI induced by lipopolysaccharide].

OBJECTIVE: To observe the effects of hydrogen sulfide (H2S) on structure and function of mitochondria of lung in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: Forty healthy male Sprague-Dawley (SD) rats were randomly divided into control group, LPS injury group, and low-, middle-, and high-dose NaHS groups, with 8 rats in each group. The rats in LPS injury group were given LPS 5 mg/kg via sublingual vein, and those in low-, middle-, and high-dose NaHS groups were challenged by LPS for 3 hours followed by intraperitoneally injection of 0.78, 1.56 and 3.12 mg/kg NaHS respectively in a volume of 2 mL/kg. The rats in control group were given 2 mL/kg normal saline via sublingual vein. The rats were sacrificed at 6 hours after model reproduction, and the lung tissues were harvested on time. The mitochondria in lung tissues were isolated with differential centrifugation. The lung mitochondria ultra structures were observed with electron microscope. The content of malondialdehyde (MDA) in mitochondria was determined with thiobarbituric acid method, and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and adenosine triphosphatase (ATPase) were determined with xanthine oxidase method. The mitochondrial activity and swelling were determined by multiskan spectrum. RESULTS: It was shown by transmission electron microscope that the mitochondrial structure in the control group was normal. The mitochondria in rat lung cells was swollen with disrupted or disintegrated cristae, the osmiophilic lamellar bodies had fused or disappeared, and rough endoplasmic reticulum degranulation phenomenon was obvious in LPS injury group. The mitochondrial damage was slightly mitigated in the low-dose NaHS group, and it was significantly mitigated in the middle-dose and high-dose NaHS groups. Compared with control group, the MDA content in lung mitochondria in LPS injury group was significantly increased (nmol/mg: 26.30±1.45 vs. 11.16±1.20), and SOD, GSH-Px, and ATPase activities were significantly decreased [SOD (U/mg): 18.78±1.13 vs. 27.44±1.97, GSH-Px (U/mg): 63.91±1.99 vs. 128.15±3.47, ATPase (U/mg): 4.83±0.25 vs. 9.92±0.65]; as well as the activity of the mitochondria was significantly decreased (A value: 0.164±0.025 vs. 0.319±0.045), and the swelling of the mitochondria was significantly increased (A value: 0.182±0.012 vs. 0.273±0.023), all with significantly statistical differences (all P < 0.01). Compared with LPS injury group, the MDA contents in low-, middle-, and high-dose NaHS groups were significantly decreased (nmol/mg: 21.89±1.23, 17.63±1.56, 12.19±1.30 vs. 26.30±1.45), and the SOD, GSH-PX, and ATPase activities were significantly increased [SOD (U/mg): 20.13±0.85, 21.38±1.22, 24.05±1.56 vs. 18.78±1.13; GSH-Px (U/mg): 82.06±1.65, 101.45±2.14, 117.80±2.12 vs. 63.91±1.99; ATPase (U/mg): 5.34±0.23, 7.06±0.37, 8.78±0.44 vs. 4.83±0.25]; as well as the activity of the mitochondria was markedly increased (A value: 0.194±0.018, 0.230±0.032, 0.297±0.038 vs. 0.164±0.025), and the swelling of mitochondria was markedly decreased (A value: 0.195±0.008, 0.219±0.017, 0.249±0.018 vs. 0.182±0.012), all with significantly statistical differences (all P < 0.05). Moreover, the protective effect of NaHS showed a dose-dependent manner. CONCLUSIONS: It could be concluded that LPS induce mitochondrial structural damage and functional impairment in rats with ALI induced by LPS, and H2S have a beneficial effect against ALI induced by LPS with decreasing the mitochondrial lipid peroxidation level and protecting the cell structure and function, and the effect is correlated with the dosage.

In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats.

BACKGROUND: Acute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI. In this study, we examined the possible roles of exogenous hydrogen sulfide (H2S) in lung mitochondria regulation in ALI rats. METHODS: The rat ALI model was induced by an intra-tongue vein Lipopolysaccharide (LPS) injection. We used sodium hydrosulphide (NaHS) as the H2S donor. We randomly divided 40 Sprague-Dawley rats into five groups: control, LPS injury, LPS + low-dose NaHS (0.78 mg • kg(-1)), LPS + middle-dose NaHS (1.56 mg • kg(-1)), and LPS + high-dose NaHS (3.12 mg • kg(-1)). Rats were killed 3 h after NaHS administration. We calculated a semi-quantitative histological index of lung injury assessments and measured the lung wet-to-dry weight ratio. We further analyzed serum for interleukin-1ß levels using enzyme-linked immunosorbent assays. We observed lung mitochondria ultrastructures with an electron microscope. We examined oxidative stress markers in lung mitochondria and the mitochondrial swelling and activity. We analyzed lung mitochondria and cytosol Cyt-c protein expression using Western blotting. RESULTS: Compared to the control group, the quantitative assessment score index, wet-to-dry weight ratios, and interleukin-1ß content in the LPS injury group were significantly increased and the mitochondrial ultrastructure damaged. Furthermore, mitochondrial activity, adenosine triphosphatease, superoxide dismutase, glutathione peroxidase, and mitochondrial Cyt-c protein expression were significantly decreased, and malondialdehyde content, mitochondrial swelling, and cytosol Cyt-c protein expression were significantly increased in the LPS injury group compared to the control group. These effects were lessened by NaHS. CONCLUSION: Exogenous H2S provided a protective effect against ALI by decreasing the mitochondrial lipid peroxidation level and protecting the cell structure in the LPS-induced rat models. Its regulatory effect on lung mitochondria is positively correlated with the dosage.