Elizabeth C. Brew

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Preconditioning may find ready applicability in humans facing scheduled global cardiac ischemia-reperfusion (IR) during bypass or transplantation, where such a maneuver is feasible before arrest. Our objective was to delineate and exploit the endogenous preconditioning mechanism triggered by transient ischemia (TI) and thereby attenuate myocardial(More)
The purpose of this investigation was to investigate the hypothesis that respiration was coupled with the mechanics of the rowing stroke. In the first part of the study, physiologic responses during incremental exercise on the variable-resistance rowing ergometer were compared in 16 untrained female subjects (U), 17 collegiate female rowers (C), and 21(More)
Preconditioning may find ready applicability in humans facing scheduled global cardiac ischemiareperfusion (IR) during bypass or transplantation, where such a maneuver is feasible before arrest. Our objective was to delineate and exploit the endogenous preconditioning mechanism triggered by transient ischemia (TI) and thereby attenuate myocardial(More)
We have reported that cardiac preconditioning against ischemia-reperfusion (IR) can be induced by transient ischemia (TI) and alpha 1-adrenoreceptor stimulation, both mediated by protein kinase C (PKC) (Mitchell, M., X. Meng, C. Parker, E. Brew, A. Harken, and A. Banerjee. Circ. Res. 76: 73-81, 1995). Our study objective was to explore the mechanism of(More)
The purpose of this experiment was to determine if cardiac preconditioning (PC) mediates protection by attenuating stunning or preventing irreversible injury. Inherent in the definition of myocardial stunning is the ability to respond to catechol stimulation after ischemia/reperfusion (I/R). Irreversibly injured myocardium cannot respond to catechols. We(More)
Inflammatory mediators of trauma and sepsis transduce cellular events through cell surface receptors initiating intricate membrane and cytosolic reaction cascades that funnel through surprisingly few checkpoints in order to provoke a cellular response. As critical care surgeons, we can explore these cell signalling systems. The purpose of this article is to(More)
Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we investigated 1) the effect of hypoxia and exogenous Ado on(More)
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