Marlene, Cheryl, Patrick (& everyone)
I found information on Wikipedia about Nitric Oxide, under the section on endothelial dysfunction.
http://en.wikipedia.org/wiki/Endothelium
"Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus. One of the main mechanisms of endothelial dysfunction is the diminishing of nitric oxide, often due to high levels of asymmetric dimethylarginine, which interfere with the normal L-arginine-stimulated nitric oxide synthesis and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in reactive oxygen species, which can impair nitric oxide production and activity via several mechanisms.[6] The signalling protein ERK5 is essential for maintaining normal endothelial cell function.[7] A further consequence of damage to the endothelium is the release of pathological quantities of von Willebrand factor, which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi."
And, I do think it's an important clue. There is a page for girl with SAA on facebook (PM me for link if interested) who, after ATG & Cyclosporine not working, got a BMT, which cured her AA but then she developed post-transplant lympoproliferative disorder and was developing huge blood clots from a very high von Willebrand factor. She is being treated with a clinical trial involving T cells at Memorial Sloan Kettering.
My suspicion is that the AA was caused by an immune dysfunction that damaged the blood vessels and endothelial cells. Her BMT resolved the immune dysfunction but not the damage to the endothelial cells.
I've been following her story because I believe my son's AA is caused by vasculitis. He's had a form of acute childhood vasculitis twice, with the relapse occurring 6 months before he was diagnosed with AA. Also, he was having symptoms of vasculitis/inflammation with his AA: 1) when his C-reactive protein goes up his numbers go down, 2) when his ANC went below 200 he'd get petechiae on his ears, regarless of platelet count, 3) during the surgery for his Port placement they inserted the port in his left chest and he broke out in purpura down his right thigh (platelets 70k, and they didn't touch him there). It also explains his rapid response to prednisone and why the response went away when the prednisone was withdrawn. Luckily vasculitis has also been shown to respond to both ATG and cyclosporine, so the treatment could work either way and seems to be working for him :-). But if he's had vasculitis three times I would like to do anything possible to ward off a fourth, or an AA relapse, or another worse manifestation of it (e.g., affecting his brain or getting the post-transplant lymphoproliferative disorder, if we needed to do a transplant.)
BTW my sons doctors don't pooh pooh my research, they just tell me "we don't know". Which is honest, they don't, so I am working to find out.
P.S. The wikipedia article also describes the platelet aggregation you were spot on about in your fish oil thread. I'm in the middle of reading an article published in Circulation Research: Journal of the American Heart Association published in May 2014 titled "Platelets as Cellular Effectors of Inflammation in Vascular Diseases".
http://circres.ahajournals.org/content/112/11/1506