TY - JOUR
T1 - Myocardial dysfunction in septic shock
T2 - Basic mechanisms and emerging concepts
AU - Hoeft, A.
AU - Mann, D. L.
PY - 1994/1/1
Y1 - 1994/1/1
N2 - There is growing evidence that myocardial dysfunction in septic shock is induced by mediators of the systemic inflammatory response syndrome, in particular by cytokines such as tissue necrosis factor-α (TNF-α) and interleukin-1 (IL-1). TNF-α produces an immediate negative inotropic effect by alteration in intracellular calcium homeostasis. Longer term effects of TNF-α and IL-1 may involve increased expression of NO synthase and decreased responsiveness of β-adrenergic stimulation. Most recently, strategies have been formulated to try and inhibit or attenuate toxic effects of TNF-α and IL-1; this has included the use of anti-TNF-α antibodies, soluble receptors for TNF-α, and recombinant IL-1 receptor antagonists.
AB - There is growing evidence that myocardial dysfunction in septic shock is induced by mediators of the systemic inflammatory response syndrome, in particular by cytokines such as tissue necrosis factor-α (TNF-α) and interleukin-1 (IL-1). TNF-α produces an immediate negative inotropic effect by alteration in intracellular calcium homeostasis. Longer term effects of TNF-α and IL-1 may involve increased expression of NO synthase and decreased responsiveness of β-adrenergic stimulation. Most recently, strategies have been formulated to try and inhibit or attenuate toxic effects of TNF-α and IL-1; this has included the use of anti-TNF-α antibodies, soluble receptors for TNF-α, and recombinant IL-1 receptor antagonists.
UR - http://www.scopus.com/inward/record.url?scp=0028058110&partnerID=8YFLogxK
U2 - 10.1097/00001503-199402000-00005
DO - 10.1097/00001503-199402000-00005
M3 - Review article
AN - SCOPUS:0028058110
SN - 0952-7907
VL - 7
SP - 26
EP - 32
JO - Current Opinion in Anaesthesiology
JF - Current Opinion in Anaesthesiology
IS - 1
ER -