ABSTRACT
Objective To study the role of D‐lactate gradient across the lung in the rapid diagnosis of pneumonia and evalua‐tion of therapeutic efficacy .Methods Patients were divided into pneumonia group (n=46) and non‐pneumonia group (n=28) in ICU .D‐lactate gradient across the lung were calculated by the difference between arterial and mixed‐venous D‐lactate concentrations before the treatment ,after 3 and 7 days of treatment .Serum procalcitonin (PCT) ,Oxygenation index ,the lung injury score (LIS) and clinical pulmonary infection score(CPIS) were recorded at the same time .Results The mean D‐lactate gradient across the lung in pneumonia group was significantly higher than that in non‐pneumonia group[(163 .84 ± 10 .72) ng/mL vs .(30 .33 ± 7 .25) ng/mL ,P<0 .01) ]before treatment .Using a cut‐off value of 106 .11 ng/mL ,D‐lactate gradient across the lung′s sensitivity for di‐agnosis pneumonia was 90 .7% and its′specificity was 75 .5% .D‐lactate gradient across the lung correlated with LIS (r= 0 .554 , P<0 .01) and CPIS(r=0 .543 ,P<0 .01) .Conclusion D‐lactate gradient across the lung correlates with lung injury and pulmonary infection positively and may be a potential biomarker for rapid diagnosis of pneumonia .
ABSTRACT
Objective To investigate the impact of Ang-1 on the septic mice′pulmonary vascular endothelial barrier function and VE-cadherin and its mechanism. Methods 80 BALB/c mice were randomly divided into NS, LPS, LPS+Ang-1, LPS+Ang-1+ Ly and Ang-1 groups (n = 16). Measure VE-cadherin, Ang-2 levels in plasma and lung permeability index (LPI).Test the total VE-cadherin of lung and the phosphorylation of VE-cadherin expression. Results Plasma Ang-2 was higher compared with NS group(P<0.01) except Ang-1 group. In LPS+Ang-1 group and LPS+Ang-1+Ly group, plasma Ang-2 was lower compared with LPS group (P <0.05). In LPS+Ang-1+Ly group, plasma Ang-2 was higher compared with LPS+Ang-1 group (P<0.01). LPI, plasma VE-cadherin and lung phosphorylation of VE-cadherin were the same with the trends of the plasma Ang-2 , but the lung total VE-cadherin showed the opposite tendency. Conclusion Through the PI3K/Akt signal transduction pathway , Ang-1 may regulate septic mice′VE-cadherin , hence the pulmonary vascular endothelial barrier function improved.