Systemic mediators released from the gut in critical illness.
OBJECTIVE
To discuss the mediators released from the gut in critical states, with emphasis on the intestinal mucosal barrier function, mediators of bacterial origin, and myocardial depressant factors.


METHODS
Relevant articles that have been published in the English language literature.


METHODS
No special study has been carried out for the present discussion.


METHODS
Information from the literature has been used to illustrate important points in the discussion.


RESULTS
Due to decreased mucosal blood flow, increased short-circuiting of oxygen in the mucosal countercurrent exchanger, and increased oxygen demand in sepsis mucosal injury develops rapidly in the gut after various forms of shock and splanchnic ischemia. In addition, due to increased generation of oxygen-derived radicals, injury may also occur with reperfusion. As a consequence of increased permeability of the intestinal mucosal barrier between the luminal content and the sterile interior milieu, increased translocation of bacteria and bacterial endotoxin occurs. In addition, cardiodepressant factors are released, as is evident from in vivo and in vitro studies. No such factor has been fully identified chemically.


CONCLUSIONS
Intestinal mucosal injury, as seen in critical illness, may induce increased translocation of bacteria and endotoxin and release of myocardial depressant factors into the circulation.
Haglund
U
U
Department of Surgery, University Hospital, Uppsala, Sweden.
D000818:Animals; D016638:Critical Illness; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000503:physiopathology; D009201:Myocardial Depressant Factor / Q000378:metabolism; D012772:Shock, Septic / Q000503:physiopathology*
D009201:Myocardial Depressant Factor