The respiratory tract is constantly exposed to environmental elements so that pathogens invade the lung easily and induce infectious disease.Most microbes could be eliminated by innate immunity and adaptive immunity.In healthy host,but in immunocompromised hosts such as HIV infection,transplant recipients,cancer,collagen vascular disease and critical illness,the lungs are more susceptible to bacteria,fungal and virus. Abstract:Summ ary: The resp iratory tract is constantly exposed to environm ental elem ents so that pathogens invade the lung easily and induce infectious d isease.Mostm icrobes cou ld be elim ina-ted by innate immun ity and adaptive immun ity.In healthy host,but in immunocomprom ised hosts such as H IV infection,trans-p lant rec ip ients,cancer,collagen vascu lar d isease and critical illness,the lungs are more susceptib le to bacteria,fungal and virus.

Objective To evaluate the value of serum galactomannan (GM) detection for invasive pulmonary aspergillosis (IPA) diagnosis. Methods The suspicious IPA patients were divided into proven,clinical and possible IPA groups. The patients excluded of IPA were recruited as controls. The serum GM concentration was detected by Platelia Aspergillus double?sandwich enzyme linked immunosorbent assay(ELISA). Re?sults In the 103 patients,there were seven cases diagnosed as proven,nineteen cases diagnosed as clinical and forty cases diagnosed as possible IPA patients. Setting 0.5 as the optimal result for GM detection,the sensitivity,specificity,positive predictive values and negative predictive values of GM were 85.7%,86.5%,55%and 97%,respectively. In non?neutropenia patients combinded with the pulmonary chronic diseases,the sensitivity, specificity,positive predictive values and negative predictive values of GM detection were 71.4%,84.4%,66.75%and 87.1%,respectively. Conclu?sion Index>0.5 for GM test could increase the sensitivity without obvious decreased specificity. GM detection could provide valuable information in patients of non?neutropenia underlying the pulmonary chronic diseases,which had a better sensitivity and specificity versus conventional diagnostic tests.

Objective: Our aim was to evaluate effects of magnesium sulfate(MgSO4) on pulmonary hypertension in patients with chronic pulmonary heart disease(CPHD). Methods: Eight patients with CPHD undergone right-heart catheterization. The parameters of hemodynamics and arterial blood gases in patients were measured before and after MgSO4 intravenous infusion(2% MgSO4,40 mg/min). Results: Mean pulmonary artery pressure(mPAP), pulmonary vascular resistance(PVR),mean systemic artery pressure(mSAP), and total systemic vascular resistance(TSVR) significantly decreased(P＜0.05) at 30 minutes after MgSO4 infusion. The decreased percentage of mPAP and PVR at 60 minute after MgSO4 infusion was 13.37% and 18.70% respectively(P＜0.05), but mSAP and TPVR decreased only by 8.15% and 7.43% respectively. The decreased degree of mPAP and PVR at 60 minutes after MgSO4 infusion significantly correlated with mPAP(r=0.712, P＜0.05)and PVR(r=0.802, P＜0.01) before MgSO4 infusion. No unfavorable effect of MgSO4 on other parameters of hemodynamics and arterial blood gases was found. Conclusion: Magnesium sulfate can attenuate pulmonary hypertension in patients with CPHD but may cause transient systemic hypotension.

Objective: Our aim was to study the effect of endothelin-1 (ET-1) on the development of chronic hypoxic pulmonary hypertension and mechanism of QF-8 (the extract of baihua qianhu, a Chinese traditional medicine) in lowering pulmonary hypertension. Methods: The indexes of hemodynamics and the levels of plasma ET-1 in systemic vein, pulmonary artery, and systemic artery in 11 patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD) were measured with right-heart catheterization and radioimmunoassay. Results: The ET-1 level in patients was significantly higher in systemic vein than that in 15 controls (P<0.01), pulmonary artery (P<0.05), and systemic artery (P<0.01). The levels of plasma ET-1 in patients had significant negative correlation with PaO2 and positive correlation with pulmonary vascular resistance index (PVRI). After taking QF-8, mean pulmonary artery pressure (mPAP) and PVRI significantly decreased, meanwhile, the levels of plasma ET-1 in systemic vein, pulmonary artery, and systemic artery also decreased by 25%, 21%, and 10%, respectively. Conclusion: Abnormality in synthesis or secretion of ET-1 may play a role in the development of chronic hypoxic pulmonary hypertension. The effect of QF-8 on pulmonary hypertension in patients with COPD may be related with its inhibition on the synthesis or secretion of ET-1.

OBJECTIVETo determine if aquaporin1 (AQP1) and aquaporin5 (AQP5) are expressed in the alveolar capillary membrane in rats. Moreover, to investigate the alteration of AQP1 and AQP5 in acute injured lungs.

METHODSThe distribution of AQP1 and AQP5 in alveolar capillary membrane were investigated by immunohistochemistry and immunoelectron microscopy with affinity-purified antibodies to human AQP1 and AQP5. To study the possibility that alveolar capillary membrane AQP1 and AQP5 undergo altered regulation, we established a rat model using alveolar instillation of lipopolysaccharide (LPS).

RESULTSImmunolabelling showed AQP1 was stained primarily in the microvascular endotheli a of normal lungs, while AQP5 was expressed in type I pneumocytes. Immunohisto chemical analysis showed a significant decrease in the expression of AQP1 and AQP5 in injured lungs at 4h-48h after LPS instillation. AQP1 protein was resumed partly at 24h after LPS instillation and steroid administration, whereas AQP5 was unchanged.

CONCLUSIONThe decreased expressions of AQP1 and AQP5 in injured lungs suggest that both of them may play a role in abnormal fluid transportation.

Animals ; Aquaporin 1 ; Aquaporin 5 ; Aquaporins ; analysis ; Immunohistochemistry ; Lipopolysaccharides ; toxicity ; Lung ; metabolism ; Male ; Membrane Proteins ; Microscopy, Immunoelectron ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; metabolism ; pathology