Microcirculatory endothelial dysfunction during endotoxemia--insights into pathophysiology, pathologic mechanisms and clinical relevance.
Alterations in microcirculatory permeability are a characteristic of early tissue injury. Moreover, tissue edema is an early indicator of tissue dysfunction, prior to organ failure, because tissue edema is associated with impaired gas exchange, arterial hypoxemia, and may also impair tissue oxygen distribution. As a result of increased microvascular permeability, plasma fluid is lost into the interstitial space, leading to hypovolemia. Currently, no effective pharmacological therapy is available to reduce increased permeability. High mortality rate in sepsis is still mainly associated with endothelial damage. In this regard platelets, besides leukocytes, play a major role for the development of microvascular hyperpermeability. This review considers endothelial cell dysfunction during endotoxemia including current insights into sepsis pathophysiology. New aspects of this complex pathogenesis are illustrated and their relevance for clinical sepsis therapy is emphasized.
Czabanka
Marcus
M
Department of Anesthesiology, University of Heidelberg, Im Neuenheimer Feld 110, D-69120 Heidelberg, Germany.
Peter
Christoph
C
Martin
Eike
E
Walther
Andreas
A
D000818:Animals; D001792:Blood Platelets / Q000502:physiology; D002448:Cell Adhesion; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D019446:Endotoxemia / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008407:Mast Cells / Q000502:physiology; D008833:Microcirculation / Q000473:pathology / Q000503:physiopathology; D009569:Nitric Oxide / Q000494:pharmacology / Q000502:physiology
D009569:Nitric Oxide