HOW DOES HEO2 INCREASE MAXIMUM EXPIRATORY FLOW IN HUMAN LUNGS
HOW DOES HEO2 INCREASE MAXIMUM EXPIRATORY FLOW IN HUMAN LUNGS
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DOI:
10.1172/jci109909
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发表时间:
1980-01-01
影响因子:
15.9
通讯作者:
WOOD, LDH
中科院分区:
文献类型:
--
作者:
MINK, SN;WOOD, LDH
The retrograde catheter technique was used to investigate the effect of HeO2 on resistance to maximum expiratory flow (.ovrhdot.Vmax) in airways subsegments between alveoli and the equal pressure point (EPP), and between EPP and the flow-limiting segment (FLS). FLS were found at the same airway site in sublobar bronchi (i.d. [inner diameter], 0.54 .+-. 0.13 cm) on both air and HeO2 in 6 human excised lungs. Static elastic recoil pressure (5 .+-. 1 cm H2O) and the lateral pressure at FLS (critical transmural airway pressure -6 .+-. 3 cm H2O) were not different on the 2 gases. .DELTA..ovrhdot.Vmax averaged 37 .+-. 8.9% and was similar to the value found in healthy subjects of similar age (66 .+-. 10 yr). EPP were located on HeO2 in peripheral airways (i.d., 0.33 .+-. 0.03 cm), and EPP on air were located more downstream. Resistance between EPP and FLS was highly density dependent. Resistance between alveoli and EPP behaved as if it were density independent, due in part to Poiseuille flow in the peripheral airways and in part to the consequent narrowing of peripheral airways on HeO2. This density-independent behavior in peripheral airways reduced .DELTA..ovrhdot.Vmax on HeO2 from its predicted maximal amount of 62%. Assuming that FLS is the choke point, these findings are consistent with wave-speed theory of flow limitation modified to include functionally density-independent pressure losses in peripheral airways. These results and conclusions are similar to those found in living dogs. They question previous interpretation of .DELTA..ovrhdot.Vmax as an index of peripheral airway obstruction, and demonstrate the utility of the wave-speed theory in explaining complicated mechanisms of expiratory flow limitation.