Lung heparan sulfates modulate K(fc) during increased vascular pressure: evidence for glycocalyx-mediated mechanotransduction.

Lung endothelial cells respond to changes in vascular pressure through mechanotransduction pathways that alter barrier function via non-Starling mechanism(s). Components of the endothelial glycocalyx have been shown to participate in mechanotransduction in vitro and in systemic vessels, but the glycocalyx's role in mechanosensing and pulmonary barrier function has not been characterized. Mechanotransduction pathways may represent novel targets for therapeutic intervention during states of elevated pulmonary pressure such as acute heart failure, fluid overload, and mechanical ventilation.

Mechano-transduction and barrier regulation in lung microvascular endothelial cells.

Alterations in endothelial permeability are a hallmark of inflammation as well as the underlying cause of many clinical syndromes. Quantifying changes in endothelial barrier properties to water and macromolecules can be an important means of assessing the degree of cellular injury and, conversely, the effect of therapies to attenuate the inflammatory cascade. We use a combination of an isolated organ system and two cell culture models to investigate mechanisms of endothelial barrier regulation under variety of experimental conditions.

Impact of vasopressin on hemodynamic and metabolic function in the decompensatory phase of hemorrhagic shock.

Objectives: To explore how the potent vasoconstrictive features of vasopressin impact the rate of cardiovascular collapse and metabolic derangements associated with prolonged hemorrhagic shock.

Design: A prospective randomized trial.

Setting: University hospital-based animal laboratory.

Influence of hemorrhagic shock followed by crystalloid resuscitation on propofol: a pharmacokinetic and pharmacodynamic analysis.

Background: Previous work has demonstrated that ongoing hemorrhagic shock dramatically alters the distribution, clearance, and potency of propofol. Whether volume resuscitation after hemorrhagic shock restores drug behavior to baseline pharmacokinetics and pharmacodynamics remains unclear. This is particularly relevant because patients suffering from hemorrhagic shock are typically resuscitated before surgery.