Sleep apnea related hypertension is a very important public health problem and is very harmful for human health and life.This article describes the concept of sleep apnea related hypertension and introduces how to recognize and make a diagnosis for sleep apnea related hypertension and how to manage it.It emphasizes the clinical significance of increasing the diagnostic rate of sleep apnea in hypertension population and 24 h ambulance blood pressure monitoring.The combination treatment for both sleep apnea and hypertension and the follow up are necessary for decreasing the prevalence of hypertension and related mobility and mortality in patients with sleep apnea.

OBJECTIVE To assess the superiority of new type bi-level positive airway pressure(Bi-PAP) in treating overlap syndrome. METHODS Sixteen cases diagnosed overlap syndrome were quickly given Bi-PAP treatment simultaneously,where their therapeutic efficacy of antibiotic,relieving spasm,diuresis and respiratory stimulant in advance was not fine.All patients were divided into new type Bi-PAP and old Bi-PAP groups based on the type of machines used. RESULTS Seven of 16 patients receiving new type Bi-PAP got remission through non-invasive mechanical ventilation.Among the other 9 patients receiving old type Bi-PAP,6 got remission through non-invasive mechanical ventilation,3 received invasive mechanical ventilation because of poor response to non-invasive mechanical ventilation. CONCLUSIONS More acute overlap syndrome patients can get remission through new type Bi-PAP without invasive mechanical ventilation and have decreased possibility of getting hospital-acquired pneumonia.

This paper introduces the concensus on the relationship between sleep apnea and cardiovascular disease reached by experts with corresponding backgrounds from Chinese Medical Association.The relationship is that of sleep apnea with hypertension,coronary artery disease,arrhythmias,and congestive heart failure,and the relationship can improve the diagnosis and treatment of these two types of diseases.

Objective To investigate the concentration changes of vascular endothelial growth factor(VEGF), nitric oxide(NO) and endothelin (ET) in elderly patients with obstructive sleep apnea syndrome (OSAS) combined with eerebrovascular disease.Methods One hundred and thirty-two subjects were divided into four groups: OSAS with cerebrovaseular disease group (OC group), OSAS without cerebrovascular disease group (O group), cerebrovascular disease without OSAS group (C group) and normal control group (N group).The concentrations of VEGF, NO and ET in the plasma were compared in each subgroup.Results The concentration of VEGF was significantly increased in OC group and O group compared with C group and N group[(195.34±56.7)ng/L, (162.34±48.7)ng/L, (156.4 4±51.8) ng/L, (114.1 ± 54.2) ng/L, F= 21.02, P< 0.05].The concentration of NO was increased gradually in OC group, C group, O group and N group[(62.3±4.9)mmol/L,(64.7±5.1) mmol/L, (66.2± 4.2)retool/L, (77.5 ± 6.8) mmol/L, F= 17.35, P<0.05], and the concentration of ET was decreased gradually in OC group, C group, O group and N group[(59.8±9.6)ng/L, (56.5±4.3)ng/L, (54.7±7.9)ng/L, (37.2±8.5)ng/L, F= 4.27, P<0.05].Conclusions The concentrations of VEGF and ET are increased and the concentration of NO is decreased in patients with OSAS.Patients with OSAS combined with cerebrovascular disease have higher VEGF and ET concentrations and lower NO concentration than in patients with simple OSAS.The results indicate that vascular endothelial dysfunction may play an important role in the development of cerebrovascular disease in patients with OSAS.

Rapid on site evaluation (ROSE) technology of interventional pulmonology includes“cytological ROSE”(C-ROSE) and“microbiological ROSE”(M-ROSE). Recently, this“ROSE”has gradually become one of core technologies in modern interventional pulmonology. In this commentary, perspectives on origin and development, classification and clini-cal value, operational approach, clinical application, and how to carry out effective work related to ROSE were summarized and remarked.

Objective To investigate the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA) supplementation on neuron apoptosis,brain edema,activation of microglia,inflammatory response and neural function after traumatic brain injury (TBI) in rats,so as to understand the protection of ω-3 PUFA in rats following TBI and its mechanism.Methods TBI model was established using Feeney's method.Ninety SD rats were randomly divided into 5 groups:sham operation group (sham group),TBI group,TBI + selective activator of c-Jun N-terminal kinase (JNK) anisomycin group (TBI + Aniso group),TBI + ω-3 PUFA supplementation group (TBI + ω-3 group),and TBI + ω-3 PUFA supplementation + JNK activation group (TBI + ω-3 + Aniso group).We measured rat behavioral outcomes by modified neurological severity score (mNSS) on day 1,3,and 7 after TBI.Brain water content was measured with wet-dry weight method.The neuron apoptosis and microglial activation (identified by specific marker IBA-1) in TBI cerebral cortex were determined by TUNEL staining and immunofluorescence.Inflammatory cytokines [tumor necrosis factor-α (TNF-α),interleukin (IL)-1α,IL-1β,and IL-6] and the JNK signaling pathway (JNK,pJNK) were tested with reverse transcription-polymerase chain reaction and Western blot,respectively.Results Compared with the sham group,the levels of brain cell apoptosis,brain edema,neuron apoptosis,and inflammatory-relatived factors (TNF-α,IL-1 α,IL-1β,and IL-6) were significantly increased in the other four groups (P ＜ 0.05).Compared with the TBl group,ω-3 PUFA supplementation reduced brain water content following TBI,especially on day 3 after TBI [(78.14 ± 0.57) ％ vs.(82.31 ± 0.81) ％,P ＜ 0.01],and improved neurological function score (P ＜ 0.05).Meanwhile,ω-3 PUFA supplementation suppressed neuron apoptosis,the activation of microglia,and the mRNA and protein expressions of inflammatory cytokines (TNF-α,IL-1α,IL-1 β,IL-6).The activation of JNK signaling pathway was also inhibited by ω-3 PUFA.Conclusion ω-3 PUFA supplementation may markedly reduce brain edema,suppress neuron apoptosis,and improve neurological outcomes after TBI in rats,possibly mediated by inhibiting JNK signaling pathway and microglial activation,reducing microglia-induced cerebral inflammatory responses,demonstrated as down-regulated expression of TNF-α,IL-1α,IL-1β,and IL-6.

Objective To establish the rat overlap syndrome (OS) model of intermittent hypoxia (IH) and emphyse-ma, explore the systematic and endothelial inflammation status, and observe the changes of endothelial progenitor cell (EPC) level in peripheral blood. Methods Sixty male Wistar rats were randomly divided into four groups:normal oxygen control group (A), IH group (B), emphysema group (C) and OS group (D). The rat model of emphysema was established by smoke ex-posure for 16 weeks. From the 13-week, pre-programmed intermittent hypoxia/re-oxygenation (IH/ROX) exposure was giv-en in the meantime of smoke exposure. After exposure, ELISA method was used to detect values of tumor necrosis factor al-pha (TNF-α) and interleukin (IL)-6 in plasma and in the endothelium of right common carotid artery. Real-time-PCR assay was used to analyze RhoA mRNA level in the endothelium of right common carotid artery. The percentage of intima-media thickness (IMT) in the all wall of right carotid artery (C-IMT%) was measured. Flow cytometry was used to detect EPC levels. Results The values of TNF-α, IL-6, RhoA mRNA and C-IMT%were significantly higher in D group than those of A, B and C groups (P<0.05). The EPC levels were significantly lower in D group than those of A, B and C groups (P<0.05). Con-clusion OS rats had more serious vascular endothelial injury than that of emphysema or IH rats. Meanwhile, the repair ca-pacity of EPC for endothelium was worse, which increased the risk of cardiovascular diseases.

Objective To investigate the effect of emphysema and intermittent hypoxia (IH) on the hepatic oxidative stress and inflammatory injury in rats. Methods Sixty male Wistar rats were randomly assigned to 4 groups, control group (A), emphysema group (B), IH group (C) and emphysema+IH group (D). Group A was normally fed. Group B was exposed to smoke, 30 min per time, twice everyday. Group C was exposed to 5%O2 30 s/Air 90 s for 8 h/d. Group D was exposed to smoke twice, about 30 min each time, and exposed 5%O2 30 s/Air 90 s for 8 h/d. After continues exposure for 8 weeks, five rats in each group were randomly selected for arterial blood gas analysis. The tissue blocks of liver was obtained for pathologi-cal scoring and measurements of liver oxidative stress in the rest 10 rats of each group. HE staining was used to calculate the mean lining interval (MLI) and mean alveolar number (MAN). The hepatic inflammatory factor interleukin-6 (IL-6), tumor necrosis factor-α(TNF-α), superoxide dismutase (SOD) activity, catalase (CAT) activity and malondialdehyde (MDA) con-centration were measured in four groups. Results Characteristics of emphysema were found in group B and group D. The values of MLI were significantly higher in Group B and group D than those of group A and group C (P<0.05). The values of MAN were significantly lower in group B and group D than those of group A and group C (P<0.05). The levels of SOD and CAT were significantly lower in group B, group C and group D than those of group A (P<0.05). And the levels of SOD and CAT were significantly lower in group D than those of group B and group C (P<0.05). The values of liver MDA were signifi-cantly higher in group B, group C and group D than those of group A, and the values were significantly higher in group D than those of group B and group C (P<0.05). The liver histological scores and the levels of IL-6 and TNF-αwere signifi-cantly higher in group B, group C and group D than those of group A, and the values were significantly higher in group D than those of group B and group C (P<0.05). Conclusion Emphysema and IH have synergistic action in causing hepatic oxidative stress and inflammation.

Objective To investigate the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA)supplementation on brain edema,autophagy response and neurobehavioral outcome after traumatic brain injury (TBI) in rats and the related mechanisms.Methods TBI rat models were established using Feeney's method.Seventy-two SD rats were divided into 4 groups using random number table:sham operation group,TBI group,ω-3 PUFA supplementation group (TBI + ω-3 group) and autophagy inhibitor 3-methyladenine group (TBI + 3-MA group) (all n =18),each group was further divided into 3 sub-groups (n =6) corresponding to 3 time points (days 1,3,and 7 after TBI).On each of the 3 time points,we measured rat behavioral outcomes with modified neurologic severity score (mNSS) tests;brain water content was measured with wet-dry weight method.The mRNA and protein expressions of autophagy-related factors (LC3-Ⅱ and Beclin-1) in TBI cerebral cortex were determined by immunohistochemistry staining,reverse transcription-polymerase chain reaction and Western blot on day 3 after TBI.Results Compared with the sham group,on days 1,3,and 7 after injuary,the TBI group,the TBI + ω-3 group,and the TBI + 3-MA group had significantly higher mNSS scores (TBI group:12.42±0.27vs.1.34±0.32,12.07±0.27vs.1.16±0.29,10.22±0.39vs.1.22±0.30;TBI+ω-3 group:12.05 ±0.23 vs.1.34 ±0.32,11.38 ±0.21 vs.1.16±0.29,8.20 ±0.21 vs.1.22±0.30;TBI +3-MA group:11.93 ±0.20 vs.1.34 ±0.32,11.09 ±0.19 vs.1.16 ±0.29,7.93 ±0.17 vs.1.22 ± 0.30;all P =0.00) and brain water content [TBI group:(79.82 ± 0.61) ％ vs.(71.87 ± 0.43) ％,(83.04±0.42)％ vs.(72.13 ±0.53)％,(75.12 ±0.72)％ vs.(71.78 ±0.38)％;TBI+ω-3 group:(76.81 ±0.63)％ vs.(71.87 ±0.43)％,(79.39 ±0.59)％ vs.(72.13 ±0.53)％,(73.86 ±0.38)％ vs.(71.78 ±0.38)％;TBI+3-MAgroup:(75.98 ±0.49)％ vs.(71.87 ±0.43)％,(77.14 ±0.46)％ vs.(72.13 ±0.53)％,(72.24 ±0.37)％ vs.(71.78 ±0.38)％;all P =0.00].The mRNA and protein expressions of LC3-Ⅱ and Beclin-1 in the brain were also significantly higher on day 3 in the TBI group,the TBI + ω-3 group,and the TBI + 3-MA group (all P =0.00).Compared with the TB1 group,on day 3 and day 7 after injury,the TBI + ω-3 group and the TBI + 3-MA group had significantly lower mNSS scores (TBI + ω-3 group:11.38±0.21 vs.12.07±0.27,P=0.04,8.20±0.21 vs.10.22±0.39,P=0.01;TBI+3-MA group:11.09±0.19vs.12.07 ± 0.27,P=0.01,7.93 ± 0.17 vs.10.22±0.39,P=0.00).Ondays1,3,and 7,compared with the TBI group,the TBI + ω-3 group and the TBI + 3-MA group had significantly lower brain water content [TBI + ω-3 group:(76.81 ± 0.63) ％ vs.(79.82 ± 0.61) ％,P =0.04,(79.39 ±0.59)％ vs.(83.04±0.42)％,P=0.01,(73.86±0.38)％ vs.(75.12±0.72)％,P=0.03;TBI+3-MAgroup:(75.98 ±0.49)％ vs.(79.82 ±0.61)％,P=0.01,(77.14 ±0.46)％ vs.(83.04 ±0.42)％,P =0.00,(72.24 ± 0.37) ％ vs.(75.12 ± 0.72) ％,P =0.02].On day 3,the TBI + ω-3 group and the TBI + 3-MA group had significantly reduced LC3-Ⅱ and Beclin-1 mRNA expression compared with the TBI group (TBI +ω-3 group:P=0.04,P =0.01;TBI +3-MA group:P =0.01,P =0.00) and protein expression (TBI+ω-3 group:P=0.01,P=0.03;TBI +3-MA group:both P=0.00).Conclusion ω-3 PUFA supplementation could markedly reduce brain edema and improve neurological functions after TBI,showing a neuroprotective effect,possibly through inhibiting TBI-induced autophagy responses.

Objective To observe the curative effect of continuous airway positive pressure ventilation (CPAP) in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and cough syncope. Methods Forty-three hospitalized patients with OSAHS and cough syncope were collected in the Department of Respiration of Tianjin General Hospital, and analyzed the related information. They were given CPAP treatment, and were divided into good compliance group (n=26) and poor compliance group (n=17) according to CPAP compliance after a half-year treatment. The apnea hypoventilation index (AHI) and c-reactive protein (CRP) were compared before and after treatment between two groups. Results The positive correlation was found between the frequency of the cough syncope and indicators of OSAHS, such as AHI, body mass index (BMI), CRP, sleepiness score (ESS) and circumference of abdomen and neck (r=0.612, 0.431, 0.224, 0.654, 0.435 and 0.344,P<0.05). All these patients were cured after the treatment of both CPAP and medication for 1 or 2 weeks. During a half-year follow-up, the cough syncope didn’t occur in those patients of good compliance group, otherwise cough syncope still happened but with less frequency in patitents of poor compliance group. Before the treatment , there was no significant difference in AHI (45.00±15.69 vs. 48.70±16.47) and CRP (3.46± 1.15 vs. 3.38±0.72) between the two groups. After treatment, AHI (26.97±14.06 vs. 48.18±15.96) and CRP (1.56±0.76 vs. 3.18± 0.78) were significantly lower in the good compliance group than those of the poor compliance group (P<0.01). Conclusion Timely and sustained treatment of OSAHS may help reduce the incidence of cough syncope and significantly improve AHI, CRP and cough symptoms.