Objective To observe the expression of angiotensin-converting enzyme( ACE) and ACE2 in rat lung and kidney at different time point after smoke inhalation injury and to explore the possible mechanism. Methods Thirty healthy male SD rats were randomly divided into five groups( n = 6 in each group) , ie. a normal control group, and 4 injury groups of 1 h, 4 h, 10 h and 24 h respectively after 30 min of dense smoke inhalation. The rats were sacrificed at different time point. Lung and kidney tissue samples were collected for measurement of lung wet/dry weight ratio( W/D) , pathological study by HE staining, and ACE and ACE2 expression by immunochemistry staining. Results The inhaled rats all displayed acute lung injury symptoms. The lung W/D in the injury groups were significantly higher compared to the normal control group ( P lt; 0. 05, P lt; 0. 01) . ACE and ACE2 were expressed on cellular membrane of normal lung and kidney. The expression of ACE in lung was increased immediately after injury and the expression of ACE2 in lung was increased at 4 h after injury. No significant changes of the expression of ACE and ACE2 in kidney were observed in the five groups. Conclusion The imbalances of expression of ACE and ACE2 in lung might play an important role in the pathogenesis of smoke inhalation injury.
Objective To study the prevalence and risk factors of chronic obstructive pulmonary disease ( COPD) and provide reliable data for COPD prevention and management. Methods By cluster-random-sampling survey, the residents aged 40 yrs or older in a community in South Bank District of Chongqing were investigated.The post-bronchodilator FEV1 /FVC lt; 0. 7 was defined as COPD. Those individuals with FEV1 /FVC lower than 0. 7 would received history inquiry, X-ray of chest and ECG to exclude other disease that could impair pulmonary function. Results 1518 residents were enrolled( 517 male and 1001 female) . The prevalence of COPD was 12. 78% ( male 23. 02% and female 7. 49% ) . The major risk factors were cigarettes smoke( OR: 2. 88, 95% CI:2. 118-3. 928) and indoor cooking smoke( OR: 1. 98, 95% CI: 1. 685-3. 317) . There were 22.06% smokers were diagnosed as COPD. Only 9. 30% patients had known themselves disease condition about chronic bronchitis,emphysema or COPD. Conclusion The prevalence of COPD in Chongqing city is significant higher than average level of the whole country and the patients have poor knowledge about the disease.
Objective To study the relationship between smoking as well as smoke cessation and lung inflammation of chronic obstructive pulmonary disease( COPD) , and its possible mechanism. Methods Thirty-two Wistar rats were randomly divided into a control group, a low-dose smoking group, a high-dose smoking group, and a smoke cessation group. The expressions of NF-κB and E-selectin in rats lung were detected by immunohistochemistry and hybridization in situ. Results The mRNA and protein expressions of NF-κB in bronchial endothelial cells of the high-dose smoking group( 0. 43 ±0. 01, 0. 41 ±0. 04) , the lowdose smoking group( 0. 41 ±0. 01, 0. 40 ±0. 01) , and the smoke cessation group( 0. 39 ±0. 01, 0. 37 ±0. 03) , were significantly higher than the control group( 0. 29 ±0. 06, 0. 28 ±0. 06) ( all P lt; 0. 05) , with the high-dose smoking group and the smoke cessation group significantly higher than the low-dose smoking group ( both P lt;0. 05) . The mRNA and protein expressions of E-selectin had the similar pattern with NF-κB. The expressions of E-selectin mRNA and protein were positively correlated with the expression of NF-κB mRNA and protein respectively ( r = 0. 80, r = 0. 89, P lt; 0. 01) . Conclusions Smoking can result in high expressions of NF-κB and E-selectin in a dose dependent manner. Smoke cessation can relieve airway inflammation and is an effective measure for preventing COPD.
ObjectiveTo retrospectively compare the clinical effects of high frequency oscillatory ventilation (HFOV) and conventional ventilation (CV) on patients with acute respiratory distress syndrome (ARDS) induced by smoke inhalation injury. MethodsForty-three patients with smoke inhalation induced ARDS were admitted in the Center Hospital of Hu Ludao between October 2004 and June 2015.Among the patients, 19 cases were treated with CV (CV group) and 24 cases were treated with HFOV (HFOV group).The clinical data were collected and compared between two groups including blood gas at certain time points (6 h, 24 h, 48 h, 96 h, and 7 d) as well as complications and prognosis. ResultsThere was no significant difference in arterial blood gas between two groups before treatment (P > 0.05).After ventilation treatment, there were significant differences in arterial blood gas parameters between two groups except arterial carbon dioxide partial pressure at 48 and 96 h.And the patients in the HFOV group improved more obviously.The hospitalization time and ventilation time in the HFOV group were significantly shorter than those in the CV group (P < 0.05).No significant difference was found between two groups in the incidences of mortality, complications or 30-day survival rate (P > 0.05). ConclusionsBoth high frequency oscillatory ventilation and conventional ventilation can improve the clinical status in patients with smoke inhalation induced ARDS.These two ventilation modes do not present any difference with respect to prognosis by present evidence.
Objective To systematically review the effectiveness and model building process of heparin treatment for animal model with smoke inhalation injury. Methods Databases including PubMed, EMbase, CBM, CNKI, VIP and WanFang Data were searched to collect animal experiments about the treatment of heparin for animal model with smoke inhalation injury from inception to November 2016. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then meta-analysis was conducted by RevMan 5.3 software. Results A total of nine studies involving 11 animal experiments were included. The results showed that building animal model with smoke inhalation injury were through burning of cotton towels or pine sawdust by sheep or rats below 40℃. The results of meta-analysis showed that there was no significant difference in mortality rate between two groups (heparin group vs. control group: RR=0.38, 95%CI 0.14 to 1.05, P=0.06; heparin plus DMSO group vs. DMSO group: RR=0.10, 95%CI 0.01 to 1.51, P=0.10). In addition, the pulmonary artery pressure (MD=–3.31, 95%CI –4.51 to –2.11, P<0.000 01), wet to dry weight ratio (MD=–0.90, 95%CI –1.19 to –0.61, P<0.000 01), and lung water content (MD=–1.18, 95%CI –1.67 to –0.70, P<0.000 01) of the experimental group were lower than those in the control group. PaO2/FiO2 after 12 hours (MD=131.00, 95%CI 59.54 to 202.46, P=0.000 3), PaO2/FiO2 after 24 hours (MD=114.00, 95%CI 60.56 to 167.44, P<0.000 1), PaO2/FiO2 after 48 hours (MD=46.00, 95%CI 20.62 to 71.38, P=0.000 4) were higher than those in the control group. However, there was no significant difference in coagulation function between both groups. Conclusion The current evidence shows that the establishment of animal model of smoke inhalation injury is still lack of standard method. Heparin can decrease pulmonary artery pressure and lung water content in animal models with smoke inhalation injury. Due to the limited quality and quantity of included studies, the above conclusions are still needed to be verified by more high quality studies.