"Why would the authors not even speculate on the effects of antithrombin???"
The purpose of the paper was to understand the sequencing of events involving the coagulation system and the inflamatory system in severe sepsis, ie septic shock, and DIC. They were interested in the event(s) triggering the fulminating hypercoagulaton and multi systems organ failure which characterises the serious and frequently fatal form. They discovered that mice who lack the PAR1 cell surface receptor which reacts to thrombin, when infused with bacterial endotoxin initially became ill but did not go on to developed the full blown condition. They also found when they treated normal mice with drugs (???) which blocked the PAR1 receptors this also conveyed protection. The drugs they used are not specified.
They also studied the effect of activation of the PAR1 receptors which went a long way in explaining why the condition is so serious. At this point they concluded. The intent of the paper was to explain the pathophysiology and not clinical.
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