Hypoxic Pulmonary Vasoconstriction Does Not Explain All Regional Perfusion Redistribution in Asthma.

RATIONALE

Regional hypoventilation in bronchoconstricted patients with asthma is spatially associated with reduced perfusion, which is proposed to result from hypoxic pulmonary vasoconstriction (HPV).

OBJECTIVES

To determine the role of HPV in the regional perfusion redistribution in bronchoconstricted patients with asthma.

METHODS

Eight patients with asthma completed positron emission tomographic/computed tomographic lung imaging at baseline and after bronchoconstriction, breathing either room air or 80% oxygen (80% O) on separate days. Relative perfusion, specific ventilation (sV), and gas fraction (Fgas) in the 25% of the lung with the lowest specific ventilation (sV) and the remaining lung (sV) were quantified and compared.

MEASUREMENTS AND MAIN RESULTS

In the sV region, bronchoconstriction caused a significant decrease in sV under both room air and 80% O conditions (baseline vs. bronchoconstriction, mean ± SD, 1.02 ± 0.20 vs. 0.35 ± 0.19 and 1.03 ± 0.20 vs. 0.32 ± 0.16, respectively; P < 0.05). In the sV region, relative perfusion decreased after bronchoconstriction under room air conditions and also, to a lesser degree, under 80% O conditions (1.02 ± 0.19 vs. 0.72 ± 0.08 [P < 0.001] and 1.08 ± 0.19 vs. 0.91 ± 0.12 [P < 0.05], respectively). The Fgas increased after bronchoconstriction under room air conditions only (0.99 ± 0.04 vs. 1.00 ± 0.02; P < 0.05). The sV subregion analysis indicated that some of the reduction in relative perfusion after bronchoconstriction under 80% O conditions occurred as a result of the presence of regional hypoxia. However, relative perfusion was also significantly reduced in sV subregions that were hyperoxic under 80% O conditions.

CONCLUSIONS

HPV is not the only mechanism that contributes to perfusion redistribution in bronchoconstricted patients with asthma, suggesting that another nonhypoxia mechanism also contributes. We propose that this nonhypoxia mechanism may be either direct mechanical interactions and/or unidentified intercellular signaling between constricted airways, the parenchyma, and the surrounding vasculature.