Efficacy and safety of macitentan for pulmonary hypertension: A meta-analysis.

INTRODUCTION: Our purpose of this study is to evaluate the effect and safety of macitentan in the treatment of pulmonary hypertension (PH). METHODS: We retrieved the safety and efficacy of macitentan treatment for PH using PubMed, the Cochrane Library, EMBASE databases and clinicaltrials.gov. The Cochrane Risk of Bias Tool was used for literature screening and quality assessment. Data analysis was conducted using RevMan 5.4.1 and Stata/SE 15.1 software. Results are presented as standardization mean differences (SMDs) and odds ratio (OR). RESULTS: Meta-analysis of seven randomized controlled trial (RCT) studies and four non-RCT studies with 2769 patients was included, involving 723 in the macitentan group and 599 in the placebo group. The results of the study showed that macitentan had effectively decreased pulmonary vascular resistance (PVR) (SMD = -0.53, 95% CI: -0.77--0.29, p < 0.05), cardiac index (CI) (SMD = 0.60, 95% CI: 0.37-0.83, p < 0.05) and N-terminal pro-brain natriuretic peptide (NT-proBNP) (SMD = -0.22, 95% CI: -0.40--0.03, p < 0.05). Furthermore, macitentan also significantly reduced PVR (SMD = -0.58, 95% CI: -0.80--0.35, p < 0.05), 6-min walk distance (6WMD) (SMD = 0.33, 95% CI: 0.15-0.50, p < 0.05), CI (SMD = 0.48, 95% CI: 0.28-0.69, p < 0.05), mean pulmonary arterial pressure (mPAP) (SMD = -0.43, 95% CI: -0.64--0.23, p < 0.05) and NT-proBNP (SMD = -0.55, 95% CI: -1.07--0.03, p < 0.05) between baseline and follow-up. The adverse reactions to macitentan were mild, with headache, anaemia and bronchitis. Other efficacy and safety outcomes did not reach statistical differences. CONCLUSION: Macitentan therapy for PH is effective and safe. The effectiveness on PVR, mPAP, mean right atrial pressure (mRAP), mortality and other indicators still needs to be further confirmed.

Clinical characteristics of 140 patients infected with SARS-CoV-2 in Wuhan, China.

BACKGROUND: Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been widely spread. We aim to investigate the clinical characteristic and allergy status of patients infected with SARS-CoV-2. METHODS: Electronic medical records including demographics, clinical manifestation, comorbidities, laboratory data, and radiological materials of 140 hospitalized COVID-19 patients, with confirmed result of SARS-CoV-2 viral infection, were extracted and analyzed. RESULTS: An approximately 1:1 ratio of male (50.7%) and female COVID-19 patients was found, with an overall median age of 57.0 years. All patients were community-acquired cases. Fever (91.7%), cough (75.0%), fatigue (75.0%), and gastrointestinal symptoms (39.6%) were the most common clinical manifestations, whereas hypertension (30.0%) and diabetes mellitus (12.1%) were the most common comorbidities. Drug hypersensitivity (11.4%) and urticaria (1.4%) were self-reported by several patients. Asthma or other allergic diseases were not reported by any of the patients. Chronic obstructive pulmonary disease (COPD, 1.4%) patients and current smokers (1.4%) were rare. Bilateral ground-glass or patchy opacity (89.6%) was the most common sign of radiological finding. Lymphopenia (75.4%) and eosinopenia (52.9%) were observed in most patients. Blood eosinophil counts correlate positively with lymphocyte counts in severe (r = .486, P < .001) and nonsevere (r = .469, P < .001) patients after hospital admission. Significantly higher levels of D-dimer, C-reactive protein, and procalcitonin were associated with severe patients compared to nonsevere patients (all P < .001). CONCLUSION: Detailed clinical investigation of 140 hospitalized COVID-19 cases suggests eosinopenia together with lymphopenia may be a potential indicator for diagnosis. Allergic diseases, asthma, and COPD are not risk factors for SARS-CoV-2 infection. Older age, high number of comorbidities, and more prominent laboratory abnormalities were associated with severe patients.

[Meta-analysis of risk factors for all-cause mortality of pulmonary thromboembolism].

OBJECTIVE: To evaluate the causes of death and risk factors of pulmonary thromboembolism. METHODS: Pubmed, English Medical Current Contents, Chinese Conference Data and Chinese Biomedical Database were searched from January 1995 up to May 2011. And the references of these studies were also examined. Observational studies were assessed according to suggestion of quality assessment with references. Randomized control trials (RCT) were assessed with Jadad scale. Software RevMan 5.1 was used to examin the heterogeneity of trials. The fixed or random effect model was employed to pool the risk ratio and 95%CI. The results were expressed with risk ratio and 95%CI. RESULTS: Thirty-five studies with a total number of 19 613 cases of pulmonary thromboembolism (PTE) were included for final analysis. The average mortality rate was (10.7 ± 7.6)% (range 0.5%-30.0%). And the following factors increased the total mortality of pulmonary embolism: right ventricular hypokinesis or dysfunction (2.18(1.64-2.89), P = 0.000), elevated D-dimer (5.19(1.93-13.96), P = 0.001), elevated cardiac troponin (cTnI) (4.01(2.77-5.81), P = 0.000), hypotension (2.76(1.25-6.09), P = 0.010), malignancy (2.65(2.01-3.50), P = 0.000), congestive heart failure (1.90(1.62-2.22), P = 0.000), chronic lung disease (1.40(1.18-1.66), P = 0.000), tachycardia (1.65(1.23-2.20), P = 0.000), immobility (1.74(1.36-2.21), P = 0.000) and age > 65 years (1.24 (1.13-1.37), P = 0.000), etc. When multiple factors co-existed, the risk of death became more obvious. CONCLUSION: Elevated D-dimer, elevated cTnI, hypotension, malignancy, right ventricular hypokinesis or dysfunction, immobility, congestive heart failure, tachycardia, chronic lung disease, age > 65 years influence the mortality rate of pulmonary embolism.

[Inhibitory effects of celecoxib combined with capecitabine on H22 hepatoma mice and its mechanism].

OBJECTIVE: To evaluate the inhibitory effect and its mechanism of celecoxib combined with capecitabine on the growth of implanted H22 hepatoma in mice. METHODS: Tumor model was established by hypodermical injection of H22 cells in BALB/c nude mice. Forty mice were equally randomly divided into 4 groups: control group, celecoxib group (receiving 100 mg/kg celecoxib), capecitabine group (receiving 755 mg/kg capecitabine), and combined treatment group (receiving 100 mg/kg of celecoxib and 755 mg/kg of capecitabine). From the third post-implantation day, each mouse was given relevant drug (or normal saline) by oral gavage. Fifteen days later, all mice were sacrificed and the tumor tissues were measured. The mRNA and protein levels of nuclear factor kappa-B (NF-ΚB) p65 and cyclooxygenase (COX)-2 in tumor tissues were detected by the quantitative polymerase chain reaction (qPCR)and Western blotting, respectively. RESULTS: The tumor inhibition rate was 30.2% in celecoxib group and 49.9% in capecitabine group, which was significantly lower than that (75.4%) in the combined treatment group (P<0.01,P<0.05, respectively). qPCR showed a significant decrease of the mRNA expression of COX-2 in celecoxib group and combined treatment group when compared with control group (P<0.001), but no significant change in NF-ΚB p65.Capecitabine had no significant effects on the mRNA expression of COX-2 and NF-ΚB p65. Western blotting showed that celecoxib and combined treatment significantly inhibited the protein expression of COX-2 and NF-ΚB p65(P<0.05), but not capecitabine. CONCLUSION: Celecoxib can enhance the antitumor effect of capecitabine by inhibiting the expressions of COX-2 and NF-ΚB p65 in mice bearing H22 implanted tumor.

[Association of genetic polymorphisms of angiotensin converting enzyme and matrix metallo proteinase-1 with idiopathic pulmonary fibrosis].

OBJECTIVE: To investigate the correlation between angiotensin converting enzyme (ACE) and matrix metallo proteinase (MMP)-1 gene polymorphisms and the risk of idiopathic pulmonary fibrosis (IPF) in a Han Chinese population from Hebei Province. METHODS: Eighty-four IPF patients and 100 controls were enrolled from the Second Hospital of Hebei Medical University. Polymerase chain reaction (PCR) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) were used to detect ACE gene insertion/deletion (I/D) polymorphism and MMP-1 polymorphism respectively. The MMP-1 polymorphism was genotyped by DNA sequence analysis. Radioimmunoassay and ELISA were used to analyzed AngII, MMP-1 and TIMP-1 levels in IPF patients and healthy controls. RESULTS: There was a significant difference between the 2 groups in allele and genotype frequency distribution of ACE Insertion/Deletion polymorphism; frequency distribution of DD genotype and D allele of IPF patients were higher than those of the healthy control group (χ(2) = 11.227, 4.318, P < 0.05). There was no difference from different genders and ages on allele and genotype frequency distribution of ACE Insertion/Deletion polymorphism. (χ(2) = 0.03 - 1.069, P > 0.05). There was no significant difference between the 2 groups in genotype and allele frequency distribution of MMP-1 1G/2G polymorphism (χ(2) = 0.94 and 0.001, P > 0.05). The AngII levels from DD genotype of both IPF patients and healthy controls were the highest, followed by the DI genotype and the II genotype. The AngII level of any genotype for ACE Insertion/Deletion polymorphism in the IPF group was higher than that in the healthy control group (all P < 0.05). The serum level of AngII, MMP-1 and TIMP-1, as well as MMP-1/TIMP-1 ratio in the IPF group were higher than those in the healthy control group (all P < 0.05). CONCLUSIONS: The ACE polymorphism might be associated with IPF, and the serum level of AngII was affected not only by the genetic background of ACE insertion/deletion polymorphism but also the environmental factors. The MMP-1 1G/2G polymorphism might be weakly associated with IPF.

Plasminogen activator inhibitor-1 promotes the proliferation and inhibits the apoptosis of pulmonary fibroblasts by Ca(2+) signaling.

AIM: Our previous investigation demonstrated that plasminogen activator inhibitor-1 (PAI-1) siRNA ameliorated bleomycin (BLM)-induced rat lung fibrosis. The present study was undertaken to explore the effect and the mechanism of PAI-1 siRNA and plasmid pcDNA on the proliferation and apoptosis of cultured fibroblasts from BLM-induced fibrotic lung tissues. MATERIALS AND METHODS: The fibroblasts from BLM-induced fibrotic lung tissue were isolated and transfected using PAI-1 siRNA and plasmid pcDNA-PAI-1. The techniques of real time RT-PCR and/or western blot were used to determine the expression of PAI-1, α-smooth muscle actin (α-SMA) (real time RT-PCR only), collagen type-1 and type-3 (real time RT-PCR only), and the levels of caspase-3, ERK and AKT signal molecules. The proliferation of fibroblasts was measured by cell cycle with flow cytometry. The intracellular concentration of Ca(2+) was examined by confocal laser microscopy. RESULTS: PAI-1 siRNA downregulated the PAI-1 mRNA expression by 70%±7% at 24h and protein expression by 73.5%±10% and 42%±3% at 48h and 72h compared to Non-specific siRNA group. Flow cytometry showed that the fibroblasts at the G(2)M+S phase were significantly reduced by 20.56±1.03% after transfecting PAI-1 siRNA and were significantly increased by 43.8±1.21% after transfecting plasmid pcDNA-PAI-1. The mRNA expressions of α-SMA, collagen type-1and type-3 were downregulated after transfecting the PAI-1 siRNA, while upregulated after the transfection of pcDNA-PAI-1. PAI-1 siRNA increased the level of caspase-3, inhibited the expressions of p-ERK and p-AKT protein molecules, while the pcDNA-PAI-1 transfection showed a reversal effect on these expressions. Intracellular Ca(2+) concentration was decreased after transfecting PAI-1 siRNA, whereas increased after transfecting pcDNA-PAI-1. CONCLUSION: PAI-1 promotes the proliferation, transforming into myofibroblasts, collagen synthesis, and inhibits apoptosis of pulmonary fibroblasts by activating Ca(2+), ERK and AKT signaling pathway. Decreasing PAI-1 expression is an available strategy in inhibiting the progression of pulmonary fibrosis.

[Altered expressions of alkane monooxygenase and hypoxia inducible factor-1α expression in lung tissue of rat hypoxic pulmonary hypertension].

OBJECTIVE: To explore the altered expressions of alkane monooxygenase (AlkB) and hypoxia-inducible factor-1α (HIF-1α) in a rat model of hypoxic pulmonary arterial hypertension. METHODS: Twenty Wistar rats were divided randomly into normal control and hypoxia groups after 1-week adaptive feeding. Hypoxia group was raised in a homemade organic glass tank with a 24-h continuous supply of air and nitrogen atmospheric mixed gas. And the oxygen concentration of (10.0 ± 0.5)% was controlled by oxygen monitoring control system. The control group was maintained in room air. Both groups stayed in the same room with the same diet. After 8 weeks, the level of mean pulmonary pressure (mPAP) was measured by right-heart catheterization, right ventricular hypertrophy index (RVHI) calculated by the ratio of right ventricle to left ventricle plus septum and hypoxic pulmonary vascular remodeling (HPSR) observed under microscope. And the levels of AlkB and HIF-1α mRNA and protein in lungs were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot. RESULTS: At 8 weeks post-hypoxia, compared with the control group [11.0 ± 0.7 mm Hg (1 mm Hg = 0.133 kPa), 0.210 ± 0.035], the levels of mPAP and RVHI in hypoxia group (33.3 ± 1.3 mm Hg, 0.448 ± 0.013) increased significantly (both P < 0.05), the expressions of AlkB mRNA and protein in pulmonary tissue decreased significantly (0.338 ± 0.085 vs 0.688 ± 0.020, P < 0.01) (0.483 ± 0.052 vs 0.204 ± 0.010, P < 0.01), and the expressions of HIF-1α mRNA and protein increased significantly (0.790 ± 0.161 vs 0.422 ± 0.096, P < 0.01) (0.893 ± 0.080 vs 0.346 ± 0.008, P < 0.01). CONCLUSION: The down-regulation of AlkB in lung tissue may increase the activity of HIF-1 to participate in the occurrence and development of pulmonary hypertension.

[Effects of PM2.5 exposure on Klebsiella pneumoniae clearance in the lungs of rats].

OBJECTIVE: To investigate the effects of PM2.5 exposure on susceptibility to Klebsiella infection and bacterial clearance, and to discuss its possible mechanisms. METHODS: Eighty-six healthy male SD rats were randomly divided into 4 groups: a control group, a Klebsiella pneumoniae infection group(infection group), a PM2.5 group and a PM2.5+ Klebsiella pneumoniae infection group (combined group) .We developed a rat model in which the animals were given Klebsiella pneumoniae, PM2.5 exposure and PM2.5 exposure followed by infection with Klebsiella pneumoniae respectively. The clinical scores were evaluated. The total mortality of each group was assessed. Bacterial load in the BALF was quantified and the infection rate of each group was assessed.Lung histopathological changes were detected by HE staining. The concentrations of IL-6 and TNF-α in serum were detected by ELISA. Cells in the BALF were counted for each group by microscopy. The changes of tracheal membrane epithelial cells were observed by scanning electron microscope. RESULTS: The total mortality in the combined group (n = 14) was higher than that in the control group (n = 0), infection group(n = 4) and PM2.5 group(n = 4). The infected cases in the combined infection group (n = 13) was higher than that in the infection group (n = 6). The total number of WBC in BALF in the combined group on the first day[(11.96 ± 0.56)×10(5)/L] and seventh day [(15.68 ± 0.81)×10(5)/L] was higher than that in the control group, the infection group and the PM2.5 group. The neutrophil number in BALF in the combined group on the first day[(5.76 ± 0.44)×10(5)/L] and seventh day [(9.41 ± 0.64)×10(5)/L] was higher than that in the control group, the infection group and the PM2.5 group. The lung pathological changes were much more severe in the combined group as compared to those in the control, the infection and the PM2.5 groups. Concentrations of TNF-α in serum in the combined group on the first day [(829 ± 90) ng/L] and the seventh day [(1055 ± 91) ng/L] were higher than those in the control group and the PM2.5 group. Concentrations of IL-6 in serum in the combined group on the first day [(1.26 ± 0.16) ng/L] and seventh day [(1.95 ± 0.18) ng/L] was higher than those in the control, the infection and the PM2.5 groups. Tracheal cilia in the PM2.5 group showed signs of disorderly arrangement, adhesion and ecclasis. CONCLUSIONS: PM2.5 exposure increased the susceptibility of the rats to Klebsiella pneumoniae infection and decreased bacterial clearance.Its mechanism may be related to impairment of the bronchial mucociliary system and interaction of cytokines.

[Meta-analysis of risk factors for recurrent pulmonary thromboembolism].

OBJECTIVE: To evaluate the risk factors of recurrent pulmonary thromboembolism (PTE) through Meta-analysis. METHODS: Chinese Journal Full-text Database, Chinese Biomedical Database, PubMed and Foreign Medical Journal Full-Text Service were searched for the paper relating to the risk factors of recurrent PTE from January 1995 to May 2011. And the references of these studies were also examined. Observational studies (cohort & case control) were assessed according to the method of quality assessment suggested within the references. Randomized control trials (RCTs) were assessed by the Jadad scale. Software RevMan 5.1 was used to examine the heterogeneity of trials. The fixed or random effect model was pooled to calculate the risk ratio (RR). And the results were expressed by RR (95%CI). RESULTS: Forty-two trials including 36 909 cases of PTE and/or deep vein thrombosis were analyzed. And the following factors were relative to recurrence: elevated D-dimer (1.77 (1.34 - 2.36), P = 0.000), idiopathic PTE (1.82 (1.61 - 2.05), P = 0.000), right ventricular dysfunction (RVD) (persistent RVD vs RVD regression (8.71 (2.38 - 31.91), P = 0.001); persistent RVD vs non-RVD (2.45 (1.26 - 4.76), P = 0.008), short anticoagulation duration (1.73 (1.32 - 2.28), P = 0.000), increased endogenous thrombin generation capacity (1.89 (1.39 - 2.56), P = 0.000), elevated factor VIII (1.96(1.40 - 2.74), P = 0.000), positive antiphospholipid antibodies (5.64 (4.09 - 7.77), P = 0.000), anti-thrombin defect (2.45 (1.26 - 4.76), P = 0.008) and males (1.47 (1.06 - 2.03), P = 0.020), etc. When multiple factors co-existed, the risk of recurrence became more obvious. CONCLUSIONS: Elevated D-dimer, idiopathic PTE and many other factors may influence the recurrence of pulmonary embolism. And most recurrent patients have two or more factors.

siRNA against plasminogen activator inhibitor-1 ameliorates bleomycin-induced lung fibrosis in rats.

AIM: Plasminogen activator inhibitor-1 (PAI-1) is involved in the progression of pulmonary fibrosis. The present study was undertaken to examine the effects on pulmonary fibrosis of silencing PAI-1 expression with small interfering RNA (siRNA) and to assess the possible underlying mechanisms. METHODS: Male Wistar rats were subjected to intratracheal injection of bleomycin (BLM, 5 mg/kg, 0.2 mL) to induce pulmonary fibrosis. Histopathological changes of lung tissue were examined with HE or Masson's trichrome staining. The expression levels of α-smooth muscle actin (α-SMA), collagen type-I and type-III, caspase-3, as well as p-ERK1/2 and PI3K/Akt in the lung tissue were evaluated using imunohistochemistry and Western blot analyses. The fibroblasts isolated from BLM-induced fibrotic lung tissue were cultured and transfected with pcDNA-PAI-1 or PAI-1siRNA. The expression level of PAI-1 in the fibroblasts was measured using real time RT-PCR and Western blot analysis. The fibroblast proliferation was evaluated using MTT assay. RESULTS: Intratracheal injection of PAI-1-siRNA (7.5 nmoL/0.2 mL) significantly alleviated alveolitis and collagen deposition, reduced the expression of PAI-1, α-SMA, collagen type-I and collagen type-III, and increased the expression of caspase-3 in BLM-induced fibrotic lung tissue. In consistence with the in vivo results, the proliferation of the cultured fibroblasts from BLM-induced fibrotic lung tissue was inhibited by transfection with PAI-1-siRNA, and accelerated by overexpression of PAI-1 by transfection with pcDNA-PAI-1. The expression of caspase-3 was increased as a result of PAI-1 siRNA transfection, and decreased after transfection with pcDNA-PAI-1. In addition, the levels of p-ERK1/2 and PI3K/Akt in the fibrogenic lung tissue were reduced after treatment with PAI-1siRNA. CONCLUSION: The data demonstrate that PAI-1 siRNA inhibits alveolitis and pulmonary fibrosis in BLM-treated rats via inhibiting the proliferation and promoting the apoptosis of fibroblasts. Suppression ERK and AKT signalling pathways might have at least partly contributed to this process. Targeting PAI-1 is a promising therapeutic strategy for pulmonary fibrosis.

[Association between genetic polymorphism of erythrocyte CR1 and the susceptibility of idiopathic pulmonary fibrosis].

OBJECTIVE: To explore the association between the erythrocyte CR1 genomic density polymorphism, A3650G site polymorphism and the susceptibility of idiopathic pulmonary fibrosis (IPF); and to investigate the correlation between the HindIII density polymorphism of CR1 gene and the quantitative levels of E-CR1 in IPF patients. METHODS: Blood samples from IPF patients (n = 64) and ethnically matched healthy controls (n = 54) were taken from a population-based case-control association study. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to identify the genotype of the HindIII restriction fragment length polymorphism of CR1 gene and SNP A3650G in two groups. Quantitative expression of CR1 on RBC membrane surface was detected by flow cytometry. RESULTS: The genotype frequencies of HH, HL and LL were 32.8% (21/64), 46.9% (30/64) and 20.3% (13/64) respectively in the IPF group, and 72.2% (39/54), 25.9% (14/54) and 1.9% (1/54) respectively in the controls. The distribution of genotype between the two groups was significantly different (χ(2) = 15.516, P < 0.05). HL + LL genotype for the HindIII polymorphism was more common in patients with IPF compared to the controls with an OR = 5.32 (χ(2) = 18.20, P < 0.05). Compared the allele frequency of A3650G sites in the IPF group with that in the control group, there was no difference from distribution in the two groups (χ(2) = 1.094, P > 0.05). The mean CR1/E numbers observed in the IPF patients was 13.46 ± 3.86, and the mean CR1/E in normal individuals was 24.33 ± 3.84 (t = 15.288, P < 0.05 vs IPF group). The levels of E-CR1 in both IPF patients and healthy controls HH genotype for E-CR1 HindIII-RFLP were significantly higher than HL genotype for E-CR1 HindIII-RFLP (t = 9.973, P < 0.05), and the levels of E-CR1 in both groups HL genotype for E-CR1 HindIII-RFLP were significantly higher than LL genotype for E-CR1 HindIII-RFLP (t = 9.973, P < 0.05). The levels of HH, HL and LL genotypes for E-CR1 HindIII-RFLP in the IPF group were significantly lower than those in the control group, respectively (P < 0.05, on average). CONCLUSION: The quantitative levels of CR1 on erythrocyte membrane was not only determined by the genetic background of E-CR1 HindIII-RFLP but also by the acquired predisposition. HL and LL genotypes of CR1 gene may be associated with IPF, and as a result individuals carrying the L allele might be a susceptible population for IPF.

Influence of auricular plaster therapy on sleeping structure in OSAS patients.

OBJECTIVE: To evaluate the therapeutic effects of auricular plaster therapy for obstructive sleep apnea syndrome (OSAS) and the influence on sleeping structure. METHODS: 45 OSAS patients were randomly divided into a treatment group of 30 cases and a control group of 15 cases for comparison of the changes in parameters of respiration and sleep at night. RESULTS: The auricular plaster therapy significantly improved the hypoventilation index, respiratory disturbance index and other respiratory parameters as well as the sleeping parameters such as the time and rate of sleep at stage I and II, and the waking time and rate. CONCLUSION: Auricular plaster therapy may show good therapeutic effects for OSAS, and with the advantages of low cost and less side effects.

[The change and significance of the cardiopulmonary exercise test parameters in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To investigate the change of exercise cardiopulmonary function in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Thirty OSAHS patients and 18 normal healthy adults (control group) were studied by cardiopulmonary exercise test (CPET). The results including maximal oxygen uptake percent predicted (Vo(2)max% predicted), oxygen uptake to work rate (Vo(2)/WR), oxygen pulse percent predicted (Vo(2)/HRmax% predicted), anaerobic threshold to maximal oxygen uptake (AT/Vo(2)max), breathing reserve (V(E)max/MVV) and ventilatory equivalents for carbon dioxide (V(E)/V(CO2)) were compared between two groups. RESULTS: The levels of Vo(2)max% predicted, AT/Vo(2)max, Vo(2)/HRmax% predicted, Vo(2)/WR, and V(E)max/MVV in the OSAHS group [(83 +/- 5)%, (44 +/- 6)%, (79 +/- 5)%, (9.3 +/- 0.6) ml.min(-1).W(-1), (73 +/- 8)%] were lower than those in the control group [(88 +/- 5)%, (49 +/- 6)%, (83 +/- 4)%, (10.9 +/- 2.3) ml.min(-1).W(-1), (79 +/- 9)%, all P < 0.05]. The levels of V(E)/V(CO2) in the OSAHS group (29 +/- 3) was higher than the control group (26 +/- 3, P < 0.05). In the OSAHS group Vo(2)max% predicted, Vo(2)/HRmax% predicted, Vo(2)/WR AT/Vo(2)max and V(E)max/MVV correlated negatively with apnea-hypopnea index (AHI, r = -0.52, -0.62, -0.59, -0.37, -0.66, P < 0.05). Vo(2)max% predicted, Vo(2)/HRmax% predicted, Vo(2)/WR, AT/Vo(2)max and V(E)max/MVV correlated with lowest oxygen saturation (LSaO(2), r = 0.60, 0.63, 0.64, 0.40, 0.59, P < 0.05). V(E)/V(CO2) correlated with AHI (r = 0.57, P < 0.01) and correlated negatively with LSaO(2) (r = -0.62, P < 0.01). CONCLUSIONS: The cardiac output of patients with OSAHS can not meet the demand of hard exercise. At the same time, there is more significant ventilation-perfusion disturbance in OSAHS patients than normal subjects. The patients' exercise cardiopulmonary function has been compromised although there are no symptoms.

[Intervention effect of tongfei mixture on nocturnal hypoxia in patients with chronic obstructive pulmonary disease].

OBJECTIVE: To study the effect of tongfei mixture (TFM, a Chinese recipe mainly consisted of angelica and rehmannia root) on nocturnal hypoxia in patients with chronic obstructive pulmonary disease (COPD). METHODS: Sixty patients with COPD of remission phase were randomly divided into 3 groups, 20 in each group. Group A was the control group; Group B, the group simply treated with oxygen; Group C, treated with oxygen and TFM. Changes of pulmonary function, diaphragm muscle mobility (DMM), 6 min walk distance (6MWD), morning arterial blood gas, nocturnal lowest oxygen saturation (LSaO2), mean blood oxygen saturation (MSaO2), the percentage of saturation lower than 90% time account for total sleeping time (SLT90%) and ultrasonocardiogram before and after treatment were observed. RESULTS: Levels of LSaO2, MSaO2 and SLT90% in Groups B and C were significantly higher than those in Group A (P<0.05, P<0.01). The lowering of PaCO2 in Group C was more significant than that in Group B (P<0.05). The mPAP level in Group C was lower, FEV1, 6MWD and DMM were improved than those in Group A and B, showing significant difference (P<0.05). CONCLUSION: Combined use of oxygen therapy and TFM could not only improve the nocturnal hypoxia, but also lower PaCO2. TFM is an important supplement of oxygen therapy.

[Clinical observation on effect of auricular acupoint pressing in treating sleep apnea syndrome].

OBJECTIVE: To study the clinical effect and mechanism of auricular acupoint pressing (AAP) in treating sleep apnea syndrome (SAS). METHODS: Forty-five patients with SAS were randomly divided in to the AAP group (30 patients) and the control group (15 patients) to observe the changes of clinical symptoms, apnea-hypopnea index (AHI), apnea index (AI), hypopnea index (HI) and minimum blood oxygen saturation (mSaO2) in night before and after treatment by multiple channel polysomnography (PSG). RESULTS: Clinical symptoms were significantly alleviated in the AAP group after treatment, with improvement in various parameters monitored by PSG (P < 0.01), showing significantly reduced AHI, AI and HI and increased mSaO2 (P < 0.01). While in the control group, no improvement was found either in clinical symptom or in PSG parameters (P > 0.05). Comparison between the two groups showed significant difference (P < 0.01). CONCLUSION: AAP is an effective treatment of SAS, it provides a facilitate, economic and safe therapy for early prevention and treatment to SAS.