Lung membrane conductance and capillary volume derived from the NO and CO transfer in high-altitude newcomers

Abstract

Acute exposure to high altitude may induce changes in carbon monoxide (CO) membrane conductance (DmCO) and capillary lung volume (Vc). Measurements were performed in 25 lowlanders at Brussels (D0), at 4,300 m after a 2- or 3-day exposure (D2,3) without preceding climbing, and 5 days later (D7,8), before and after an exercise test, under a trial with two arterial pulmonary vasodilators or a placebo. The nitric oxide (NO)/CO transfer method was used, assuming both infinite and finite values to the NO blood conductance (θNO). Doppler echocardiography provided hemodynamic data. Compared with sea level, lung diffusing capacity for CO increased by 24% at D2,3 and is returned to control at D7,8. The acute increase in lung diffusing capacity for CO resulted from increases in DmCO and Vc with finite and infinite θNO assumptions. The alveolar volume increased by 16% at D2,3 and normalized at D7,8. The mean increase in systolic arterial pulmonary pressure at rest at D2,3 was minimal. In conclusion, the acute increase in Vc may be related to the increase in alveolar volume and to the increase in capillary pressure. Compared with the infinite θNO value, the use of a finite θNO value led to about a twofold increase in DmCO value and to a persistent increase in DmCO at D7,8 compared with D0. After exercise, DmCO decreased slightly less in subjects treated by the vasodilators, suggesting a beneficial effect on interstitial edema.

TLNO/TLCOratio is not the end of the road

“…The annual rate of decline in FEV1 in the present study was slightly greater (-90 mL in the placebo group and -123 mL in the doxycycline group) compared with that observed in the re-evaluation performed by our group (-73 mL in patients that received doxycycline) and with that identified in the study of TaveiraDaSilva and colleagues (-75 mL) [1,8]. Can we assign a greater decline in FEV 1 identified in the doxycycline group in the present study to a greater impairment in baseline pulmonary function?…”

“…It could be suggested that both conductances might be lower than these in vitro values; however, it seems highly unlikely that both in vitro values were overestimated, and no published hCO value is ,0.58 mmHg?min -1 in normoxia. Interestingly, using the aforementioned hNO/hCO leads to increased Dm [8], reaching the morphometric value of WEIBEL et al [10]. This reasoning has sharp consequences for the interpretation of both TLCO and TLNO as, if the hNO/hCO value of 7.7 is confirmed, it would lead us to consider that TLCO is mainly dependent on Vc, as TLNO would be equally dependent on Dm and Vc.…”

“…It can be demonstrated using the ROUGHTON and FORSTER [4] equation for the two gases that the TLNO/TLCO ratio cannot be greater than hNO/hCO, i.e. 7.7 [8]. As the upper normal value of TLNO/TLCO reaches approximately 5.5-6.0 in most reports [2,9], a hNO value ,4.5 or a hCO value .0.58 are unlikely as they would lead to a decrease in hNO/hCO to ,7.7.…”

The centenary (2015) of the transfer factor for carbon monoxide (TLCO): Marie Krogh's legacy

“…Subsequently, physiological studies, involving simultaneous nitric oxide (NO) and CO uptake, have shown that 80% of the resistance to CO transfer from alveolar gas to intracapillary Hb (∼1/T LCO .sb) lies in the red cell itself 17 18. Thus, it is not unreasonable to describe the T LCO as a ‘window on the pulmonary microcirculation’ 19…”

“…These two groups, from Cambridge, UK17 and Bordeaux, France,18 have since shown that, for NO, 35–40% only of the transfer resistance lies in the red cell (80% for CO). Thus, T LNO .sb is more weighted to the alveolar and capillary surface area, that is, true diffusion, than to the red cell.…”