You know, I was watching Dexter and drinking coffee, and I just figured something out:
I read the posts from the more seasoned altitude providers about CCB's, Phosphodiesterase inhibitors and presumably nitro not working for HAPE, and I couldn't lay it to rest. Why would nitro work for cardiogenic PE and not HAPE?
Then it hit me: It isn't about pulmonary hypertension when you're having a heart attack. It's about
pump failure. So by decreasing venous return to the heart, you decrease the work load on the LV, which decreases the whole CHF effect.
Seems if the sole cause of the PE (pulmonary edema, not pulmonary embolism) is a decreased extravascular pressure gradient and pulmonary vasoconstriction caused by hypoxia, decreasing venous return to the heart really dosen't seem to help that much, at least while you're within theraputic levels.
So, I conclude that nitro has a minimal effect on pulmonary vasculature, which makes sense because these vessels do what they want to begin with. Take the head for example, hypoxia causes
vasodilation, wheras the opposite happens in the lungs. So it dosen't seem suprising then, that the pharmacodynamics of conventional vasodilators wouldn't work accross the board on different sets of plumbing.
Now all I gotta do is wait for DARPA to catch up.
