The researchers examined 16 climbers who had previously experienced HAPE and 14 who had not. They placed catheters in the subjects' pulmonary arteries¿which take blood from the heart to the lungs¿to measure blood pressure. They also gauged the permeability of the pulmonary capillaries. Their goal was testing a common belief that HAPE results when the lower air pressure at high altitudes causes lung capillaries to swell or when the capillaries begin to leak as a result of inflammation. The researchers examined the subjects at a low altitude of 490 meters and then at 4,559 meters 24 hours later.
"We could not find any signs of inflammation," lead author Marco Maggiorini, a physician at the University of Zurich in Switzerland, says. "We did find elevated pressure in the capillaries, which leads to water in the lungs, or pulmonary edema." It turned out that subjects who had experienced HAPE had higher average pulmonary artery pressure and capillary pressure than those who had never developed the condition. The team also found that among those susceptible to HAPE, the ones who actually developed HAPE all had higher pulmonary capillary pressures than the rest.
Based on these findings, Maggiorini suggests that pulmonary edema can be treated with vasodilators to lower pulmonary capillary pressures. "The condition is strictly related to a lack of oxygen in the air when climbers or hikers reach certain altitudes," he explains. "As soon as you give oxygen or a vasodilator, the pressure goes down."