[A study on the end criteria of forced vital capacity curve in adults].

Objective: To explore the end criteria of forced vital capacity(FVC) curve in adults. Methods: A multicenter cross-sectional study was performed in Zhongshan Hospital Affiliated to Fudan University, the First Affiliated Hospital of Fujian Medical University, and the Third Affiliated Hospital of Inner Mongolia Medical University from January 2017 to August 2017. A consecutive sample of subjects who completed the spirometry test and FVC curves met end criteria of no volume change (<0.025 L) for ≥ 1 s were qualified in this study. Subjects were divided into a normal group (n=610), an obstructive group (n=536), and a restrictive group(n=306) according to pulmonary function test results. The FET values in different groups were compared. The side effects in the 3 groups and the diagnostic accuracy, specificity and security of different FET in the obstructive group were assessed. Results: The FET values of the normal group, the obstructive group, and the restricted group were (4.00±1.07) s, (8.08±1.56) s and (2.97±0.76) s respectively, and the 95% CI of FET in the 3 groups were between 3.88-4.12 s, 7.02-10.14 and 2.21- 3.73 s (F=2 263.80, P<0.01). When the exhalation platform was used as the standard of FVC curve, the adverse reaction rate in the normal group and the restricted group were 1.1% and 1.3% respectively, lower than the rate of 17.2% in the obstructive group (χ(2)=92.73, χ(2)=48.49 respectively; all P<0.05). In the obstructive group, 7 s as the ending criterion had similar incidence of adverse reactions to 6 s (χ(2)=0.01, P=0.93). With further extension of expiration time, the incidence of adverse reactions increased significantly. In the obstructive group, the sensitivity of FEV(1)/FEV(7) was 99.25%, higher than that at FEV(1)/FEV(6) (χ(2)=4.06, P=0.04), and the specificity of diagnosis was very similar and 100%. Conclusions: FET was variable in subjects with different lung function status. It is not appropriate to use a fixed FET≥ 6 s as the end criterion of spirometry for adults. For patients with normal lung function or restrictive lung function defect, exhalation platform should be used as the end of exhalation standard. For patients with obstructive lung function defect, an FET of up to 7 s is appropriate.

[Role of TNF-α in vascular remodeling in rats with chronic thromboembolic pulmonary hypertension].

Objective: To analyze the relationship between TNF-α and pulmonary vascular remodeling in order to explore the pathogenesis of CTEPH. Methods: Autologous blood clots were repeatedly injected into the left jugular vein of rats to establish the CTEPH model. Then mean pulmonary artery pressure (mPAP), histopathology, the plasma level of TNF-α, and the expressions of mRNA and protein of TNF-α in pulmonary artery were measured. Results: In the experiment group, the mPAP and vessel wall area/total area (WA/TA) ratio gradually increased as emblism extended, and increased significantly compared with the sham operation group. The plasma TNF-α concentration in the experimental group increased significantly (P<0.05). The TNF-α proteins expressed in pulmonary artery in the 1-week, 2-week, and 4-week subgroups of experimental group increased significantly compared with the sham operation group (1.62±0.08 vs 0.85±0.12, P<0.05; 1.85±0.08 vs 0.89±0.13, P<0.05; 1.37±0.12 vs 0.91±0.15, P<0.05, respectively). Immunohistochemical results showed that TNF-α expression was higher in pulmonary artery endothelial cells of the experimental group compared with the sham operation group. The expression of pulmonary artery TNF-α protein was positively related with mPAP (r=0.605, P<0.01), and with WA/TA (r=0.629, P<0.01). The expression of serum TNF-α was positively related with that of pulmonary artery TNF-α protein (r=0.721, P<0.01). Conclusion: A rat model of CTEPH can be established by repeatedly introducing autologous blood clots into the pulmonary artery with injecting TXA. Thrombosis induced higher expression of TNF-α in pulmonary arterial endothelial cells, and released into the blood. TNF-α may play an important role in the development of CTEPH, especially by contributing to vascular remodeling and PH.