Why the study?
Does intravenous BAY 58-2667 improve hemodynamics and renal function in a model of tachypacing-induced severe congestive heart failure?
Population
Model of tachypacing-induced severe congestive heart failure
Design
Preclinical
Authors
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Hypothesis-generating for BAY 58-2667 in experimental HF; human trials required before clinical consideration.
Does intravenous BAY 58-2667 improve hemodynamics and renal function in a model of tachypacing-induced severe congestive heart failure?
In an experimental model of severe heart failure, the soluble guanylate cyclase activator BAY 58-2667 improved cardiac hemodynamics and renal blood flow without neurohumoral activation.
Boerrigter et al. (2007) studied this question.
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