A narrative review of historic and current approaches for patients with difficult venous access: considerations for the emergency department.

Introduction: Timely placement of vascular access devices is critical during emergent clinical situations; however, challenges in peripheral access can be a common occurrence. Historically, emergency teams have used various approaches to gain peripheral vascular access in situations where traditional means were not feasible; these options have included peripheral venous cutdown, ultrasound-guided peripheral intravenous catheters (PIVs), longer PIVs, central catheters, and intraosseous devices. Each of these options have associated strengths and limitations depending on the clinical situation.

Alcohol-use disorders in the critically ill patient.

Alcohol abuse and dependence, referred to as alcohol-use disorders (AUDs), affect 76.3 million people worldwide and account for 1.8 million deaths per year.

Hypoxia inducible factor-1: regulation by nitric oxide in posthypoxic microvascular endothelium.

Microvascular endothelial cells provide a critical regulatory interface between blood constituents and tissue. Hypoxia inducible factor-1 (HIF-1) is a key transcription factor required for expression of hypoxia-dependent genes. We employed a model of hypoxia and reoxygenation (H/R) using the dermal microvascular endothelial cell line HMEC-1 to examine the effects of altered oxygen concentrations on microvascular HIF-1 expression and nitric oxide (NO) formation.

Atypical mechanism of NF-kappaB activation during reoxygenation stress in microvascular endothelium: a role for tyrosine kinases.

The transcription factor nuclear factor kappaB (NF-kappaB) regulates genes that contribute to acute inflammatory reactions in cytokine-activated endothelium. Tumor necrosis factor activates NF-kappaB through serine phosphorylation, induced by inhibitor kappaB kinases (IKK), and subsequent degradation of inhibitor kappaB (IkappaB). In contrast to cytokine stress, our studies show that oxidative stress, generated by exposure to hypoxia followed by reoxygenation (H/R), failed to activate IKK in human microvascular endothelial cells (HMEC-1).

Reoxygenating microvascular endothelium exhibits temporal dissociation of NF-kappaB and AP-1 activation.

Alterations of cellular redox balance in microvascular endothelium results in changes of essential cell functions. These alterations may arise, in part, due to modifications in the pattern of gene expression produced by transcription factor activation. Endothelium subjected to hypoxia/reoxygenation becomes redox imbalanced, thereby leading to activation and perhaps production of a proinflammatory state.