Why the study?
Does endotoxin (LPS) depress contractility in isolated rat hearts via TNF-alpha synthesis?
Population
Isolated rat hearts
Comparison
Perfusion with endotoxin for 180 minutes, alone… vs null
Design
Preclinical
Follow-up
180 minutes
Authors
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Hypothesis-generating for TNF-alpha/ceramidase targeting in septic cardiomyopathy; should not change clinical practice without human data.
Does endotoxin (LPS) depress contractility in isolated rat hearts via TNF-alpha synthesis?
Endotoxin depresses myocardial contractility by inducing TNF-alpha synthesis and activating the sphingomyelinase pathway, a process facilitated by Cox-2-derived thromboxane A2.
Grandel et al. (2000) studied this question.
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