Key result
Red blood cells in experimental sepsis models accumulate NO adducts, including S-nitrosohemoglobin, and spontaneously stimulate systemic vasodilation through a cGMP-dependent mechanism.
Why the study?
Do red blood cells mediate systemic vasodilation through NO-dependent mechanisms during sepsis?
Population
Experimental models of endotoxemia and surgical sepsis
Design
Preclinical
Authors
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Hypothesis-generating for RBC NO signaling in human sepsis; prospective studies required before clinical consideration.
Do red blood cells mediate systemic vasodilation through NO-dependent mechanisms during sepsis?
Red blood cells directly mediate systemic hypotension during sepsis through NO-dependent mechanisms involving the formation of S-nitrosohemoglobin.
Crawford et al. (2004) studied Sepsis. Experimental models of endotoxemia and surgical sepsis was evaluated on Formation of NO adducts in RBCs and vasodilation. Red blood cells in experimental sepsis models accumulate NO adducts, including S-nitrosohemoglobin, and spontaneously stimulate systemic vasodilation through a cGMP-dependent mechanism.
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