Objective To explore the association between CRP and circadian variation of blood pressure in both hypertensive and normotensive old population.Methods The 82 patients with essential hypertension (EH) and 79 normotensive adults were enrolled in this study. Serum high sensitive CRP (hsCRP) level was tested by fluorescence immunoassay technology. The 24-hour ambulatory monitor of the level and variability of blood pressure was carried out. Multivariable linear regression models were run to adjust the age, gender, body mass index, blood sugar, blood fat,smoking history and baseline blood pressure for analyzing the association between hsCRP and circadian variation of blood pressure.Results ( 1 ) The variability of systolic blood pressure during daytime,nighttime and 24-h our periods were higher in EH group than in control group (P＜0.01 or P＜0. 05), the variabilities of diastolic blood pressure were also significantly higher than in control group (P＜0. 05), the dipping ratios of nocturnal systolic, diastolic and mean artery pressure were all less than in contrast group (all P＜0.05). (2) The hsCRP was obviously higher in EH group than in control group [(5.44± 1.78)mg/L vs. (3.03±0. 72) mg/L, P＜0. 01]. (3) The hsCRP had positive associations with diastolic blood pressure variability during daytime (r= 0. 492, P＜0. 001 ), nighttime (r=0.240, P=0.048), and 24-hour (r=0.271, P=0.030). The variability in diastolic blood pressure predic ted the level of hs CRP(r=0.660, R2=0.436, P＜0.001). (4) In control group, no significant association was found between CRP and variation of blood pressure.Conclusions The BP variability and serum CRP in EH patients are obviously higher than in normotensive patients,however, the nocturnal BP dipping ratio is less than in normotensive patients. Furthermore, the level of serum hsCRP in EH patients is positively associated with the variation of blood pressure, especially for variation of diastolic blood pressure.

Objective To explore the effects of polyclonal antibody to lipopolysaccharide binding protein (pLBPab) on IL 10 and IL 18 mRNA expressions of alveolar macrophages in lipopolysaccharide LPS induced acute lung injury in rats. Methods A total of 40 male Wistar rats were randomly divided into 5 groups: normal control (A), LPS treated group (B), group of pLBPab preconditioning at 30 min before injection of LPS (C), group of treatment with LPS and pLBPab (D), and group of pLBPab preconditioning at 30 min after injection of LPS (E). mRNA expressions of IL 10 and IL 18 in the alveolar macrophages in each group were measured by semi quantitative reverse transcription polymerase chain reaction (RT PCR). Results The IL 10 and IL 18 mRNA expressions were highly increased respectively in the alveolar macrophage (AM?) stimulated with single LPS, but they were significantly decreased in the AM? after stimulation with LPS + pLBPab, particularly stimulation with pLBPab 30 min before LPS injection. Conclusion pLBPab can decrease the mRNA expressions such as IL 10 and IL 18 by alveolar macrophages in acute lung injury in rats induced by LPS, and LBP antibody could be used to cure some diseases such as SIRS, acute lung injury, ARDS, and septic syndrome.

OBJECTIVE: To investigate the classification and incidence of acid-base disturbance (ABD) in the patients with post-traumatic multiple organ dysfunction syndrome (MODS). METHODS: A total of 119 patients with MODS were examined with arterial blood gas analysis and serum electrolytes detection for 675 times in this study. RESULTS: Different types of ABD existed in 647 times out of 675 times (95.9%) of blood-gas analyses. There were 270 times (41.7%) of simple ABD, 271 times (41.9%) of double ABD and 106 times (16.4%) of triple ABD. Among which, 404 times (62.4%) were in respiratory alkalosis (RAL), 332 times (51.3%) in metabolic acidosis (MA), 227 times (35.1%) in metabolic alkalosis (MAL) and 167 times (25.8%) in respiratory acidosis (RA). In this study, 79 cases (66.4%) out of 119 cases with MODS died from these kinds of ABD. CONCLUSIONS: It suggests that in the early stage of MODS, RAL with or without hypoxemia may exist, and later on, MA or even triple ABD may occur. In order to detect and correct the primary disorders as early as possible, it is important to keep the balance of hydrolyte. The treatment of primary diseases is also important. Disorders of acid-base balance were corrected according to pH standard values, anion gap (AG) and the potential [HCO(3)(-)] were also calculated simultaneously. When pH was more than 7.50 or lower than 7.20, it is necessary to give drugs of acidity or alkalinity to the patients with ABD to maintain pH value within a normal range.

0.05). VIP, however, could inhibit the Con A-induced proliferation of T-cells from control subjects more significantly than that from asthmatics (P0.05). The cAMP level in T-cells, however, increased more significantly in the control group than that in the asthmatic group after the treatment of VIP or NaF (P0.05). CONCLUSION: Inhibition effect of VIP on Con A-induced proliferation of T-cells was less in asthmatics than in control subjects, which may be related to insufficiency of Gs ? coupled VIP receptor on T-lymphocytes in asthmatics.

AIM: To observe the effects of dexamethasone and interleukin-10 (IL-10) on the release of proinflammatory cytokines, tumor necrosis factor-?(TNF-?), IL-6 and activation of transcriptional factors, nuclear factor-?B(NF-?B), activator protein-1 (AP-1) and cAMP response element binding protein (CREB) in cultrued human peripheral blood mononuclear cells (hPBMC). METHODS: The hPBMC were divided into control group, lipopolysaccharide (LPS) stimulated group, dexamethasone and IL-10 treated group. The contents of TNF-? and IL-6 in supernatant were mensured by ELISA. The activity of NF-?B, AP-1 and CREB of nuclear abstract were analyzed by electrophoretic morbility shift assay (EMSA). RESULTS: The content of TNF-? was significantly increased 1 hour after LPS stimulation, and it was significantly inhibition by dexamethasone and IL-10. The contents of IL-6 and IL-10 were significantly increased after LPS stimulation for 12 hours. The production of IL-6 was still inhibited by dexamethasone and IL-10, but the production of IL-10 was not affected by dexamethasone. The activities of NF-?B, AP-1 and CREB were significantly increased 1 hour after LPS stimulation. Dexamethasone and IL-10 significantly ihibited their activities, but the effects of dexamethasone was stronger than that of IL-10. CONCLUSIONS: LPS induces the release of several pro and anti- inflammatory cytokines and induces the activation of several transcriptional factors in hPBMC. Dexamethasone and IL-10 can inhibite the production of proinflammatory cytokines TNF-?, IL-6 and the activation of NF-?B, AP-1 and CREB. Dexamthasone has more significant inhibitory effect on AP-1 and CREB than IL-10.

AIM: To investigate the regulatory effects of lipopolysaccharide binding protein(LBP)on activation of p38 signaling pathway induced by lipopolysaccharide(LPS)in alveolar macrophages. METHODS: The LBP from actue phase rat serum was purified by ammonium sulphate precipitation, Bio-Rex70 resin and the MonoQ column. Rat alveolar macrophages were exposed to LPS (0 01 mg/L or 1 mg/L) the various concentrations of LBP(0 mg/L, 0 01 mg/L, 0 1 mg/L,1 mg/L and 10 mg/L) Western blotting were used to detect phospho-p38 in alveolar macrophages RESULTS: SDS-PAGE analysis indicated that the purified preparation of rat LBP showed homogeneity and the molecular weight was 60 kD.The binding of lipopolysaccharide to mononuclear cells were enhanced by purified rat LBP. Stimulation of rat alveolar macrophages with LPS at concentration of 0.01 mg/L was LBP dependent. LBP at concentrations up to 1 mg/L was able to increase the activation of p38. However , when LBP concentrations were further increased to 10 mg/L, the phosphorylation levers of p38 were lower as compared with that in the presence of 1 mg/L. Stimulation of rat alveolar macrophages with LPS at concentrations of 1 mg/L was LBP-independent. CONCLUSION: The activation of p38 induced by LPS at lower concentration(0.01 mg/L ) was LBP-dependent, meanwhile, LPS at higher concentration (1 mg/L ) was LBP-independent.

Changes of pulmonary ?_1-and ?-adrenergic receptor (?_1-AR and ?-AR)during endotoxin-induced acute lung injury in rates were oberved to find out the rela-tionship between them and the mechanism of change. Results showed that there was amarked decrease of B_max of both ?_1-AR and ?-AR by 35% and 43% respectively, dur-ing acute lung injury. The down regulation of ?-AR might be one of causes of acutelung injury while that of ?_1-AR seems to be a protective response. Active oxygen playedan important role in endotoxin-induced down regulation of AR in the rat lungs. The increa-sed level of norepinephrine and epinephrine was not the main factor that initiate the downregulation of AR. Intravenous injection of tumor necrosis factor (5?10~6U/kg ) exerts noiafluence on the changes of pulmonary AR in rats.

AIM: To study the effect of IFN-? inhalation on the anti-infection ability of the lungs in the immunocompromised host. METHODS: The immunological factors in the immunocompromised rats and the immunocompromised rats administrated IFN-? via aerosol were investigated after 1, 3, 7 days when they were injected Candida albicans via tracheal The Canidda albicans count of the left lung was also determined after 7 days when injecting pathogen. RESULTS: The Canidda albicans count of the left lung in IFN-? group was significantly less than that of control group. The phagocyting and bactericidal percentages, Ia antigen expression percentages, the levels of TNF-?, IL-1? and IL-6 in the culture supernatant of the AM, the activity of IFN-? and TNF-? in BALF (except the TNF-? on 7 th day) in IFN-? group were markedly higher than those in control group. The expression of IFN-? and IL-1? pulmonary tissues in IFN-? group was higher than that in control group. The expression of TNF-? in IFN-? group was less than that in control group. The expression of IL-6 was no changes between two groups. The levels of IFN-?, IL-1? and IL-6 in the blood (except IL-1? on 3 rd day), and the killing ability of the lymphocytes in blood had no difference between two groups. CONCLUSION: Administration of IFN-? via aerosol obviously enhanced the anti-infection ability of the lungs in the immunocompromised host, but has no influence on the whole body cellular immunity.

The changes of erythrocytic membrane band 3 protein and intraery-throcytic and extrar rythrccytic gases and electrolytes were studied in 69 cases of cor pulmonale and 50 normal subjects.It was found that in the patients of cor pulmonale accompanied with type Ⅱ respiratory failure,the relative low level of erythrocytic membrane band 3 protein and the restriction of HCO-3/Cl-exchange were the factors to aggravate CO2 retention and respiratory acidosis,relative intraerythrocytic alkalosis resulted from the relative increase of intra-erythrocytic HCO-3([HCO-3]),and prompt adminstration of oxygen to cor pulmonale patients with hypoxemia could not only improve extraerythrocytic acid-base imbalance but also increase intraerythcocytic P5O2 and the tissue capacity to store oxygen.

Arterial blood gases,intraerythrocytic pH(pHi),2,3-diphosphoglycerate,standard P50(P50(aid))and in vivo P50(P50iv)were determined in 54 patients with cor pulmonale and in 23 normal subjects.It was found that there was no significant change of pHi but the difference between pHi and extraerythrocytic pH was decreased.P50aid was decreased(P