ABSTRACT
The pulmonary circulation changes profoundly at high altitude as pulmonary hypertension appears. Modest pulmonary hypertension at high altitude may be beneficial in some circumstances, but severe pulmonary hypertension is nearly always detrimental. On arrival at altitude, acute hypoxia raises pulmonary arterial pressure, and with the chronic hypoxia of continued residence, pressure rises even more. But the relationship between the acute and the chronic hypoxic responses is far from clear. We hypothesize that the key to the magnitude of the pulmonary hypertension at altitude is how the pulmonary arteriolar walls thicken in the transition from arrival to chronic residence. Understanding this transition is difficult because both acute hypoxic vasoconstriction and chronic thickening of the arteriolar walls are extremely variable within and between species, and the mechanisms for either are only dimly seen.
