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Cardiac systolic function is depressed after rewarming from 25°C.
Myocardial function is depressed even in the early hyperdynamic phase of sepsis [ 53].
Myocardial function is depressed in sepsis and has a significant impact on patient outcome (Rudiger et al., 2013).
For example, polymorphonuclear leukocyte function is depressed; leukocyte adherence, chemotaxis and phagocytosis may be affected; and antioxidant systems involved in bactericidal activity may also be impaired.
In early sepsis myocardial function is depressed as: DpDt max and SVI lay down at basal time and they do not increase during the study, SVV% improves, the DpDt max ITBVI correlation is depressed during the fluid challenge and the cardiac response to dobutamine test is impaired.
Respiratory function is depressed and may be temporarily suspended during induction.
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Echocardiography demonstrated that cardiac function was depressed in diabetic mice, but HDAC inhibition resulted in a significant functional improvement in STZ-injected mice.
During reperfusion, Ca2+ transient amplitude recovered fully, but d[Ca2+]i remained elevated and LV function was depressed, indicative of Ca2+ overload.
Both groups assessed the degree to which LV systolic function was depressed with a good and very good agreement (group I: κ 0.69, 95%% CI 0.60 0.79; group II: κ 0.82, 95%% CI 0.73 0.91; full details can be found in Additional file 2).
T-cell function was depressed by adult thymectomy and sublethal irradiation, or by treatment with antilymphocyte serum (ALS).
However, administration of anesthetics would have a potential risk of deteriorating cardiovascular variable, since myocardial function was depressed after brain death [ 1, 4].
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