An early HMGB1 rise 12 hours before creatinine predicts acute kidney injury and multiple organ failure in a smoke inhalation and burn swine model.

Background: Acute kidney injury (AKI) and multiple organ failure (MOF) are leading causes of mortality in trauma injuries. Early diagnosis of AKI and MOF is vital to improve outcomes, but current diagnostic criteria rely on laboratory markers that are delayed or unreliable. In this study, we investigated whether damage associated molecular patterns such as high-mobility group box 1 (HMGB1), syndecan-1 (SDC-1) and C3a correlate with the development of trauma-induced AKI and MOF.

Alpha 1-adrenergic receptor activation releases vasopressin and oxytocin from perfused rat hypothalamic explants.

Norepinephrine and the alpha-agonist phenylephrine in concentrations of 10(-5) to 10(-3) M prompted the release of radioimmunoassayable vasopressin (up to 150 pg/min) and oxytocin (up to 20 pg/min) from intraarterially perfused explants of rat basal forebrain. Drug effects were markedly reduced or abolished in the presence of the non-specific alpha-antagonists phentolamine and phenoxybenzamine, and the specific alpha 1-antagonist prazosin. In concert with recent in vivo and in vitro electrophysiological observations, these data imply that endogenous noradrenergic pathways to magnocellular neurosecretory cells are excitatory, mediated through activation of their alpha 1-receptors, thereby enhancing the release of both vasopressin and oxytocin in the neurohypophysis.