Patients undergoing cardiac surgery with cardiopulmonary bypass are at risk of developing organ failure. The development of organ failure is only in part understood, although it is generally accepted that derangements in the host immune and coagulation responses contribute to its progression. A common factor is a microvascular dysfunction. The vascular endothelium holds a central position in the regulation of fluid transport. Inflammatory mediators activate the endothelium, fueling a proinflammatory host response as well as procoagulant processes. These changes result in shedding of the glycocalyx, endothelial hyperpermeability, vascular leakage, edema formation, and may lead to disturbed microcirculatory perfusion. As microcirculatory perfusion is essential for tissue delivery of oxygen and nutrients, disturbances in microcirculatory perfusion may result in a self-reinforcing process of organ dysfunction.
Microvascular dysfunction is observed in patients undergoing cardiac surgery with cardiopulmonary bypass. Hyperactive inflammatory and coagulation responses disturb microcirculatory perfusion, which subsequently leads to organ failure. This process, leading to organ failure, is aggravated by fluid accumulation in the interstitium, which compresses tissue and impairs microcirculatory perfusion even further. The pathophysiology is however complex and not well understood. The aim of this Research Topic is to highlight the vascular endothelium as a relevant player in the development of organ dysfunction in patients undergoing cardiac surgery.
We invite investigators to submit original research and review articles including research on patients, animals as well as in vitro studies. The areas of interest include, but are not limited to:
• Endothelial function and injury
• The glycocalyx
• Microcirculatory perfusion
• Disturbances of coagulation and platelet function
• The effect of cardiopulmonary bypass and the effect of fluid resuscitation on the above-described conditions
• Interventions targeting the above-described conditions
Patients undergoing cardiac surgery with cardiopulmonary bypass are at risk of developing organ failure. The development of organ failure is only in part understood, although it is generally accepted that derangements in the host immune and coagulation responses contribute to its progression. A common factor is a microvascular dysfunction. The vascular endothelium holds a central position in the regulation of fluid transport. Inflammatory mediators activate the endothelium, fueling a proinflammatory host response as well as procoagulant processes. These changes result in shedding of the glycocalyx, endothelial hyperpermeability, vascular leakage, edema formation, and may lead to disturbed microcirculatory perfusion. As microcirculatory perfusion is essential for tissue delivery of oxygen and nutrients, disturbances in microcirculatory perfusion may result in a self-reinforcing process of organ dysfunction.
Microvascular dysfunction is observed in patients undergoing cardiac surgery with cardiopulmonary bypass. Hyperactive inflammatory and coagulation responses disturb microcirculatory perfusion, which subsequently leads to organ failure. This process, leading to organ failure, is aggravated by fluid accumulation in the interstitium, which compresses tissue and impairs microcirculatory perfusion even further. The pathophysiology is however complex and not well understood. The aim of this Research Topic is to highlight the vascular endothelium as a relevant player in the development of organ dysfunction in patients undergoing cardiac surgery.
We invite investigators to submit original research and review articles including research on patients, animals as well as in vitro studies. The areas of interest include, but are not limited to:
• Endothelial function and injury
• The glycocalyx
• Microcirculatory perfusion
• Disturbances of coagulation and platelet function
• The effect of cardiopulmonary bypass and the effect of fluid resuscitation on the above-described conditions
• Interventions targeting the above-described conditions
