PubMed · 12588719
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Peter D Bridge, Sheila A McKenzie. 2003-02-15. Time for standardization.. https://doi.org/10.1164/ajrccm.167.4.957
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Airway resistance using the interrupter technique (Rint) can be measured using commercial devices which employ different algorithms for estimating pressure change. We aim to describe differences in Rint due to algorithm. We compared Rint and change in Rint after bronchodilator, using four algorithms to estimate pressure change following interruption: 1) two-point back-extrapolation to interruption from points 70 msec and 30 msec from interruption, and similarly 2) to 15 msec from interruption, 3) at two-thirds from interruption, and 4) near end-interruption. Flow was measured immediately before interruption. Our subjects were 39 asymptomatic children 2-5 years old with previous intermittent wheeze. Rint differed significantly with algorithm. Geometric mean Rint (95% confidence interval (CI)) for algorithms 1-4 were 1.21 kPa x l(-1) x sec (1.18-1.24 kPa x l(-1) x sec), 1.31 kPa x l(-1) x sec (1.28-1.34 kPa x l(-1) x sec), 1.57 kPa x l(-1) x sec (1.54-1.61 kPa x l(-1) x sec) and 1.71 kPa x l(-1) x sec (1.67-1.75 kPa x l(-1) x sec), respectively. Measurement of change in R(int) following bronchodilator (BDR) did not differ on average with algorithm. Geometric means (95% CI) for BDR measurements for algorithms 1-4 were 29.9% (26.0-34.0%), 30.4% (26.4-34.5%), 32.9% (28.8-37.1%), and 31.7% (27.6-35.8%), respectively. However, measurement of change in individuals could differ by up to 40%, depending on algorithm. In conclusion, there are significant differences in Rint, depending on algorithm used to estimate pressure change. Measurement of change in Rint is unaffected on average, although in individuals there could be significant differences. Each laboratory should state its method and use the same algorithm for longitudinal and group data.
Protease-activated receptors (PARs) are widely distributed in human airways, and recent evidence indicates a role for PARs in the pathophysiology of inflammatory airway disease. To further investigate the role of PARs in airway disease, we determined the expression and function of PARs in a murine model of respiratory tract viral infection. PAR-1, PAR-2, PAR-3, and PAR-4 mRNA and protein were expressed in murine airways, and confocal microscopy revealed colocalization of PAR-2 and cyclooxygenase (COX)-2 immunostaining in basal tracheal epithelial cells. Elevated levels of PAR immunostaining, which was particularly striking for PAR-1 and PAR-2, were observed in the airways of influenza A/PR-8/34 virus-infected mice compared with sham-infected mice. Furthermore, increased PAR-1 and PAR-2 expression was associated with significant changes in in vivo lung function responses. PAR-1 agonist peptide potentiated methacholine-induced increases in airway resistance in anesthetized sham-infected mice (and in indomethacin-treated, virus-infected mice), but no such potentiation was observed in virus-infected mice. PAR-2 agonist peptide transiently inhibited methacholine-induced bronchoconstriction in sham-infected mice, and this effect was prolonged in virus-infected mice. These findings suggest that during viral infection, the upregulation of PARs in the airways is coupled to increased activation of COX and enhanced generation of bronchodilatory prostanoids.
The aim of the study was to detect changes in pulmonary function following ligation of a patent ductus arteriosus (PDA). Pulmonary function was recorded in 16 newborns (birth weight 1,081 +/- 166 g, gestational age 27.6 +/- 1.7 weeks) before and after ligation. No change in resistance of airways or mean airway pressure was observed. We found an increase in dynamic compliance (Cdyn) of 77% (p < 0.01), in tidal volume (TV) of 29% (p = 0.004), and in minute ventilation (MV) of 17% (p < 0.01) after the procedure. We demonstrated that pulmonary function improves after surgical ligation of the PDA. Because of considerable variation in intubated and spontaneously breathing premature newborns, we recommend the analysis of three main parameters: Cdyn, TV and MV for estimation of pulmonary mechanics in these infants.