The medicine of critical disease is a clinical discipline that gradually sprang up in the late 1960s.Yet at present controversy still exists as to whether the discipline should be regarded as a separate one and it has not been ranked among the separate disciplines listed by the State Educational Committee. The authors, however, give an account of the customers and the cunent situation of disciplinary development of the discipline of critical disease from the petspective of a discipline. They also offer an account of the organizational structure and the form of staff of ICUs,pointing out that ICUs have 3 subjects structurally and are divided into CategoriesⅠ,Ⅱand Ⅲ. Except for ICUs in a few hospitals that are up to the level of Category Ⅱl, ICU s in most hospitals in China are lower than or just up to the level of Category Ⅰ. Then the authors give an introduction to the three forms of ICU management: open, semi-open and closed.

To evaluate availability of permissive hypercapnia (PHC) in patients with severe acute respiratory distress syndrome (ARDS). Method: To observe the influence of different tidal volumes (V_T) on pulmonary mechanics and hymodynamies in 10 patients with severe ARDS. Result : PHC was induced by decreasing VT from 10-12 ml/kg(routine V_T) to 6-8 ml/kg (small V_T). Arterial oxygen pressure and saturation remained unchanged, but pulmonary venous mixture increased(P

Objective: To observe the effect of cooling on systemic and regional oxygen metabolism in febrile critically ill patients. Method: Twenty-five critically ill patients with fever were cooled by ice blankets or by ibuprofen/indomethacin. Oxygen metabolism in whole body and regional organ and hemodynamics were measured. Result: As the temperature was reduced form 38.9?1.1℃ to 37.8?1.5℃,HR,cardiac index (CI),oxygen delivery (DO_2I),and oxygen consumption (VO_2I) decreased significantly,but gastric intramucosal pH increased from 7.26 to 7.37 and the PCO_2 difference between gastric rnucosa and arterial blood decreased markedly. PO_2 and oxygen content in cardiac coronary venous blood and oxygen exrtaction remained unchanged. Conclusion: After cooling the febrile pateints,CI, DO_2I and VO_2I decrease but tissue hypoxia can be improved.

Objective To study the effects of permissive hypercapnia (PHC)on cardiovascular system, oxygen metabolism and gastrointestinal function with acute respiratory distress syndrome(ARDS). Methods In 18 sheep with LPS induced ARDS, hemodynamics, oxygen metabolism and gastrointestinal intramucosal pH(pHi)were observed at different tidal volume(V T).Results PHC was induced by decreasing V T from 16 ml/kg to 4 7ml/kg.Compared with those at V T 16 ml/kg, cardiac index decreased significantly in PHC (P

The medicine of critical disease is a clinical discipline that gradually sprang up in the late 1960s. Yet at present controversy still hats as to whether the discipline should be regarded as a separate one and it has not been ranked among the separate disciplines listed by the State Educational Committee. The authors, however, give an account of the customers and the current situation of disciplinary development of the discipline of critical disease ho the perspective of a discighne. They also offer an account of the organizational structure and the form of staff of ICUs, pointing out that ICUs have 3 subjects structurally and are divided into CategoriesⅠ,Ⅱ and Ⅲ. Except for ICUs in a few hospitals that are up to the level of Category n, ICUs in most hospitels in China are lower than or just up to the level of CategoryⅠ. ho the authorss give an introduction to the ho formsn of ICU management open, semi-opened-cpc ana closed.

Acute respiratory distress syndrome (ARDS) is a common clinical critical condition of the respiratory system, with a high fatality rate and lack of effective drug treatment, hence it is a global medical problem to be solved urgently. Recently, with the in-depth research on extracellular vesicles (EVs) at home and abroad, more and more evidences suggest that EVs play a critical role in the initiation, development and progression of ARDS and have potential clinical application value. The role of different cells derived EVs in ARDS will be reviewed in this paper.

Objective To observe the regularity of expression changes in CD80 in peripheral blood, lung and splenic dendritic cells (DCs) in mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and its correlation with lung inflammation. Methods Twelve C57BL/6 mice were randomly divided into two groups, namely control group and ALI group, with 6 mice in each group. LPS (2 mg/kg) was intra-tracheal instilled in mice to reproduce ALI model, while the control mice received intra-tracheal administration of phosphate buffer saline (PBS) instead. The mice were sacrificed 6 hours after model reproduction, lung tissues were collected, and lung coefficient was calculated (lung wet weight/body weight ×100%). The pathological changes were examined under optical microscope after hematoxylin and eosin (HE) straining, the severity of lung injury was evaluated by the Smith score. Interleukin-6 (IL-6) level was determined by enzyme-linked immunosorbent assay (ELISA). After single-cell suspensions were isolated from the lung and spleen, the level of CD80 on DC in peripheral blood, lung and spleen was assessed by flow cytometry (FCM). The correlation between CD80 positive DC number and the severity of lung injury was analyzed by Spearman correlation method. Results Compared with control group, LPS-induced ALI resulted in a significant increase in lung coefficient [(0.67±0.04)% vs. (0.52±0.02)%, P < 0.05], and the levels of IL-6 were significantly enhanced (pg/mg: 2 712±475 vs. 335±168, P < 0.05). Histologically, widespread alveolar wall thickening caused by congested, severe hemorrhage in the interstitium and alveolus, and marked and diffuse interstitial infiltration with inflammatory cells were observed in ALI group. In contrast, no histological alteration was observed in the control group. In addition, the lung injury scores were markedly higher in ALI group than those in the control group (5.10±0.24 vs. 0.60±0.12, P < 0.05). It was shown by FCM analysis that there was a gradual but significant increase trend of CD80 positive dendritic cells number in blood, lung, and spleen in both control mice and ALI mice. However, no significant differences in the number of peripheral blood CD80 positive DCs were found between control group and ALI group [(3.3±1.5)% vs. (5.1±2.1)%, P > 0.05]. In contrast, there were a low but significantly higher percentage of CD80 positive DCs in the lung and spleen in ALI group than that in control group [Lung: (9.6±2.5)% vs. (3.6±1.2)%, spleen: (25.2±4.7)% vs. (9.0±3.6)%, both P < 0.05]. It was shown by the Spearman correlation analyses that respiratory CD80 positive DCs number was significantly positively correlated with IL-6 level in the lung (r = 0.761, P = 0.042) and the Smith score (r = 0.752, P = 0.047). Conclusions There is a significantly higher percentage of CD80 positive DCs in the lung and spleen in ALI mice, and a significantly positively correlation between respiratory CD80 positive DCs number and IL-6 level in the lung or the Smith score, which suggests elevated expression of CD80 on dendritic cells seems to play an important role in the pathogenesis of acute lung injury.

Objective To investigate the effects of direct hemoperfusion with polymixin B-immobilized fiber (DHP-PMX) in patients with sepsis. Methods We searched Pubmed, Embase, Web of Science databases and identified relevant randomized controlled trials (RCT) from January 1995 to May 2010. Meta-analysis of DHP-PMX on mortality and levels of endotoxin in patients with sepsis were conducted using the methods recommended by the Cochrane Collaboration. Results Eleven RCTs were included.Eight of them included the mortality of patients (sample size: 211 DHP-PMX and 178 conventional medical therapy). In total, the mortalities of patients with sepsis in DHP-PMX group and conventional group were 37.4% (79/211) and 68.5% (122/178) respectively. Compared with the conventional medical therapy,DHP-PMX appeared to significantly reduce mortality ( OR =0.24,95% CI 0.16-0.38 ,P ＜0.000 01 ). The results were similar when two RCTs enrolling patients with methicillin resistant staphylococcus aureus (MRSA) infections were excluded( OR =0. 27,95% CI 0. 17-0. 45, P ＜0. 000 01 ). When the analysis was limited to the nine studies that reported 28- to 30-day mortality, results were unchanged( OR =0. 29,95% CI 0.17-0.48 ,P ＜0.000 01 ). Six RCTs had the available data of endotoxin. The level of endotoxin decreased 31 ng/L(95% CI 22.46-39.55 ) after DHP-PMX therapy, and the decreasing was statistically significant (P＜0. 000 01 ) ,while the level of endotoxin in patients of conventional group did not change (P =0.94).Conclusions This study suggests a favorable effects of DHP-PMX on mortality and endotoxin decreasing in patients with sepsis. However, lack of enough cases and blinding need to be considered. Further investigation with large sample of high quality RCTs is needed.

Objective To investigate the activation of nuclear factor-κB(NF-κB),which was stimulated by angiotensin-Ⅱ(AngⅡ)through classical pathway in human pulmonary microvascular endothehal cells(HPMEC).Method The experiment was divided into two groups:in Ang Ⅱ group,HPMECS were incubated with 10-6mol/L AngⅡ for 0,0.5,1,2 and 4 hours,respectively;in losartan group,HPMEC was pretreated with 10-6mol/L losartan(inhibitor of AngⅡ type 1 receptor)for 1 hour,and then stimulated with 10-6mol/L AngⅡ for 2 hours,and the nucleax protein and the cell plasma protein were prepared by lysis and centrifugation.Electrophoretic mobility shift assay(EMSA)was used to detect the NF-κB DNA binding activity.The inhibitor of κBa(IκBα)was detected by Western blotting.The data were expressed as(x±s)and analyzed with one way analysis of variance.A P value less than 0.05 indicated significant difference.Results Compared with the activity of NF-κB at 0 h (100.0±25.1)after AngⅡstimalation,the activity increased significantly at 0.5 hour(144.5±16.1,P＜0.05),and reached peak value at 2 hours(270.1±27.2,P＜0.05).The concentration of IκBα at 0 hours was 44.4%±2.1%,decreased markedly at 0.5 hours(38.9%±3.6%,P＜0.05),and to the lowest level at 2hours(32.6%±2.3%,P＜0.05).The activity of NF-κB(115.4±10.7)and the concentration of IκBα(43.6%±3.7%)in losartan group had ilo significant difference with AngⅡ group at 0 h(P＞0.05).The activity of NF-κB and the concentration of IκBα in losartan group had significant difference with AngⅡ group at 2hours.Conclusions NF-κB can be activated through classical pathway,which stimulated by AngⅡ in HPMEC.

Objective To investigate the changes in circulatory and pulmonary monary angiotensinⅡin rats with acite lung injury(ALI)and explore the role of angiotensinⅡin ALI.Method Thirty S-D rats were randomly divided into control group(n=6)and ALI group(n=24).The ALI group was further divided into four subgroups of observation at various intervals,3,6,9 and 12 hours after administration of lipopolysaccharide (LPS)into the femoral vein(each n=6).The indices rate,blood gas analysis,wet weight/dry weight(W/D)ratio of lung lobes,and pathological changes were successively observed at 3,6,9,and 12 hours after injury.The content of angiotensinⅡin lung tissue and blood plasma were detected at above set intervals by radioimmunoassay.Data of these assays were analyzed by one-factor analysis of variance.Results Compare with the control group,pH and PaO2 of arterial blood in ALI group decreased significantly(P＜0.05)at all intervals and PaCO2 of arterial blood in ALI group decreased significanfly(P＜0.05).at all intervals and PaCO2 of arterial blood and lung W/D weight ratio increased significantly(P＜0.05),and scores of lung histopathology denoted the lung injuried(P＜0.01).After injury of lung,angiotensin Ⅱ content increased markedly in lung homogenate and blood plasma (P＜0.05).Angiotensin Ⅱ content in blood plasma reached peak value at 9 hours,and content of angiotensin Ⅱ in lung homogenates kept on increasing at allintervals of observation.Conclusions A large amount of angiotensin Ⅱ releases into lung tissue and blood plasma during ALI,suggesting systemic and pulmonary rennin-angiotensin systems are activated.