Mechanisms in acute septic cardiomyopathy: evidence from isolated myocytes.
Although often not considered, the heart is one of the targets of multiple organ failure in sepsis and septic shock, with myocardial depression being a prominent component of this "acute septic cardiomyopathy". Hypotheses concerning the etiology of this depression are increasingly elucidated on a cellular level, including dysfunction of the beta-adrenoceptor/G protein/adenylate cyclase system, calcium channel blockade by cardiodepressant factor, contractile impairment by activated leucocytes, as well as inhibition of protein synthesis by Pseudomonas exotoxin A. In the search for "mechanisms of myocardial depression in sepsis", isolated cardiomyocytes may play a role as research tools with respect to: a) discrimination between direct and indirect cardiodepressant effects; b) identifying not only the acute, but also chronic toxin- and mediator-induced cardiodepression; c) clarification of the mechanism of action of cardiodepressant bacterial toxins and sepsis mediators; d) establishment of in vitro models of leucocyte-mediated cardiodepression in sepsis.
Werdan
K
K
Müller
U
U
Reithmann
C
C
Pfeifer
A
A
Hallström
S
S
Koidl
B
B
Schlag
G
G
D000208:Acute Disease; D000818:Animals; D009202:Cardiomyopathies / Q000378:metabolism* / Q000503:physiopathology; D002469:Cell Separation; D016207:Cytokines / Q000378:metabolism; D005098:Exotoxins / Q000494:pharmacology; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D007239:Infections; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011549:Pseudomonas; D011943:Receptors, Adrenergic, beta / Q000378:metabolism
D016207:Cytokines; D005098:Exotoxins; D011943:Receptors, Adrenergic, beta