Collateral ventilation may protect against high-altitude pulmonary hypertension.
We propose that the pulmonary hypertension developed by cattle and swine at high altitude is associated with their lack of collateral ventilation. We reason that if collateral ventilation helps keep interregional oxygen tensions homogeneous, then in its absence, local ventilation-perfusion balance must rely on arterial constriction; the additional work causes arterial walls to be more muscular at low altitude, a characteristic of cattle and swine that appears prerequisite for the development of pulmonary hypertension at high altitude. In contrast, species with collateral ventilation, e.g., dogs, have thin-walled pulmonary arteries and therefore can not sustain pulmonary vasoconstriction at altitude. Sheep, however, challenge the hypothesis, because their thick lobular septae should block collateral ventilation, yet they have thin pulmonary arteries and resist high-altitude hypertension. We measured collateral ventilation by determining how long it takes air injected into isolated segments to escape. Cattle and swine had no collateral ventilation (time constants greater than 30 s), whereas dogs and sheep had collateral ventilation (time constants less than 0.8 s). These data support the hypothesis that only species without collateral ventilation develop pulmonary hypertension at high altitude.