Abstract
Abstract : In this issue of Critical Care Medicine, Guarido et al (1) present their fascinating work in a model of endotoxemia in rats. Consistent with prior studies, they found that vasopressin could increase blood pressure in animals refractory to phenylephrine. What is provocative about this work is the presumptive mechanism for these findings. In septic animals, this improvement in blood pressure could not be explained by improvements in cardiac function or vasoconstriction from large vessels. The effect appeared to be a result of vasoconstriction within the renal vascular bed as evidenced by decreased renal blood flow (RBF) in vivo and increased renal vascular perfusion pressure in vitro. These effects were attenuated by Y-27632, implying that signaling via the Rho-A/Rho-kinase pathway plays a role. Presumably, this decrease in renal perfusion could potentially result in acute kidney injury (AKI), a syndrome that has been associated with increased mortality in the ICU setting (2). The implication is that in the setting of refractory shock, similar physiology may apply to patients resulting in an increase in AKI with vasopressin.
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