Hi Jesse,
These are great questions you ask.
For the first, increased inflamation might well help get ATIII on scene, but then you are already behind the ball to a degree. Hopefully there will be enough ATIII present in the lymphatic tissue prior to leakage to have good effect. A secondary hope would be that even if ATIII is not present in sufficient quantity to act to limit inflammation in the lymphatic tissue, that having sufficient intravascular ATIII present will be sufficient to help mediate (if not completely stop) DIC to the patient's benefit.
The HMS library doesn't carry the journal cited as #3 in support of the lack of ATIII efficacy (which gives you an idea of what kind of a rag it might be). Looking at the title, it simply looks like a review of APC in sepsis, so I imagine it is simply a tired recounting of the previous heparin-flawed ATIII/sepsis trials. I don't give it much cred.
I give much credit to the Nature author for the speed of his reply!
Best,
MTB
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