Acute hyperglycemia increases sepsis related glycocalyx degradation and endothelial cellular injury: A microfluidic study.

Background: Hyperglycemia promotes vascular inflammation; however its effect on endothelial dysfunction in sepsis is unknown. Microfluidic devices (MFD) may closely mimic the in vivo endothelial cell microenvironment. We hypothesized that stress glucose concentrations would increase sepsis related endothelial injury/activation.

Rapid Detection of Clostridium difficile Toxins in Serum by Raman Spectroscopy.

Background: Clostridium difficile infection (CDI) is due to the effects of toxins, toxin A and toxin B on the host. Severe CDI is associated with systemic signs of infection. Animal models of CDI demonstrate a strong correlation between systemic toxemia and the occurrence of severe disease.

Acute hyperglycemia exacerbates trauma-induced endothelial and glycocalyx injury: An in vitro model.

Background: Early hyperglycemia is associated with higher mortality in trauma and predicts multiple organ failure. Endothelial cell (EC) injury and glycocalyx (GC) degradation occur following traumatic shock and are key factors in the development of trauma-induced coagulopathy and result in impaired microvascular perfusion and accompanying organ failure. Acute hyperglycemia has been shown to result in the loss of the GC layer, EC inflammation, and activation of coagulation in vivo.

Excess sodium is deleterious on endothelial and glycocalyx barrier function: A microfluidic study.

Background: Hypernatremia is a common problem affecting critically ill patients, whether due to underlying pathology or the subsequent result of hypertonic fluid resuscitation. Numerous studies have been published, suggesting that hypernatremia may adversely affect the vascular endothelial glycocalyx. Our study aimed to evaluate if high sodium concentration would impair the endothelial and glycocalyx barrier function and if stress conditions that simulate the shock microenvironment would exacerbate any observed adverse effects of hypernatremia.

Microfluidics: A high-throughput system for the assessment of the endotheliopathy of trauma and the effect of timing of plasma administration on ameliorating shock-associated endothelial dysfunction.

Background: Early resuscitation after trauma-hemorrhagic shock with plasma rather than crystalloid may ameliorate systemic endothelial cell (EC) injury and dysfunction (endotheliopathy of trauma). We postulated that endothelial-lined microfluidic networks would be a useful platform to study the EC activation/injury under flow conditions to mimic trauma-hemorrhagic shock. We then used the microfluidic system to further characterize the protective effects and optimal timing of plasma infusion on the development of "endotheliopathy of trauma" in our model.

Hydrogen peroxide ingestion with injury to upper gastrointestinal tract.

Hydrogen peroxide is a common over-the-counter solution that has developed a growing body of literature regarding toxic ingestion. Intentional ingestion of high concentration hydrogen peroxide for health purposes has gained popularity in certain patient populations; purported benefits are due to the increased oxygen released into the blood stream. We present for evaluation one such case with associated imaging that presented to our urban medical center.

The temporal response and mechanism of action of tranexamic acid in endothelial glycocalyx degradation.

Background: The endothelial glycocalyx (GCX) plays an important role in vascular barrier function. Damage to the GCX occurs due to a variety of causes including hypoxia, ischemia-reperfusion, stress-related sympathoadrenal activation, and inflammation. Tranexamic acid (TXA) may prevent GCX degradation.

Disparate effects of catecholamines under stress conditions on endothelial glycocalyx injury: An in vitro model.

Background: Geriatric trauma patients have high circulating norepinephrine (NE) levels but attenuated release of epinephrine (Epi) in response to increasing severity of injury. We hypothesized that NE and Epi have different effects on the endothelial and glycocalyx components of the vascular barrier following shock.

Methods: Human umbilical vein endothelial cells (HUVEC) were treated with varying concentrations of NE or Epi and exposed to simulated shock conditions (HR).

Early tranexamic acid administration ameliorates the endotheliopathy of trauma and shock in an in vitro model.

Background: Systemic vascular endothelial injury is a consequence of trauma (T)/hemorrhagic shock (HS) which results in disturbances of coagulation, inflammation, and endothelial barrier integrity. The effect of T/HS on the endothelium (endotheliopathy of trauma [EoT]) is of intense research interest and may lead to EoT-directed therapies. Administration of tranexamic acid (TXA) in trauma patients is associated with a survival benefit and fewer complications if given early after injury.