Liver Endothelial Cell Dysfunction Occurs Early Following Hemorrhagic Shock and Persists Despite Crystalloid Resuscitation

1996 ◽  
Vol 63 (1) ◽  
pp. 241-247 ◽  
Author(s):  
Ping Wang ◽  
Zheng F. Ba ◽  
Andrew Biondo ◽  
Irshad H. Chaudry
Keyword(s):  
Endothelial Cell ◽  
Hemorrhagic Shock ◽  
Endothelial Cell Dysfunction ◽  
Cell Dysfunction ◽  
Liver Endothelial Cell

SELECTIVE MICROVASCULAR ENDOTHELIAL CELL DYSFUNCTION IN THE SMALL INTESTINE FOLLOWING RESUSCITATED HEMORRHAGIC SHOCK

Shock ◽  
1998 ◽  
Vol 10 (6) ◽  
pp. 417-422 ◽  
Author(s):  
Todd M. Fruchterman ◽  
David A. Spain ◽  
Mark A. Wilson ◽  
Patrick D. Harris ◽  
R. Neal Garrison
Keyword(s):  
Small Intestine ◽  
Endothelial Cell ◽  
Hemorrhagic Shock ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Dysfunction ◽  
Cell Dysfunction ◽  
Microvascular Endothelial

scholarly journals Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

2017 ◽  
Vol 232 (1) ◽  
pp. R27-R44 ◽  
Author(s):  
D S Boeldt ◽  
I M Bird
Keyword(s):  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Cell Function ◽  
Endothelial Cell Dysfunction ◽  
Hypertensive Disorders Of Pregnancy ◽  
Endothelial Cell Function ◽  
Vascular Adaptation ◽  
Cell Dysfunction ◽  
Maternal Adaptation ◽  
Flow Through

Maternal vascular adaptation to pregnancy is critically important to expand the capacity for blood flow through the uteroplacental unit to meet the needs of the developing fetus. Failure of the maternal vasculature to properly adapt can result in hypertensive disorders of pregnancy such as preeclampsia (PE). Herein, we review the endocrinology of maternal adaptation to pregnancy and contrast this with that of PE. Our focus is specifically on those hormones that directly influence endothelial cell function and dysfunction, as endothelial cell dysfunction is a hallmark of PE. A variety of growth factors and cytokines are present in normal vascular adaptation to pregnancy. However, they have also been shown to be circulating at abnormal levels in PE pregnancies. Many of these factors promote endothelial dysfunction when present at abnormal levels by acutely inhibiting key Ca2+ signaling events and chronically promoting the breakdown of endothelial cell–cell contacts. Increasingly, our understanding of how the contributions of the placenta, immune cells, and the endothelium itself promote the endocrine milieu of PE is becoming clearer. We then describe in detail how the complex endocrine environment of PE affects endothelial cell function, why this has contributed to the difficulty in fully understanding and treating this disorder, and how a focus on signaling convergence points of many hormones may be a more successful treatment strategy.

Role of glutathione redox cycle in TNF-α-mediated endothelial cell dysfunction

1995 ◽  
Vol 117 (2) ◽  
pp. 179-188 ◽  
Author(s):  
Michal Toborek ◽  
Steven W. Barger ◽  
Mark P. Mattson ◽  
Craig J. McClain ◽  
Bernhard Hennig
Keyword(s):  
Endothelial Cell ◽  
Redox Cycle ◽  
Endothelial Cell Dysfunction ◽  
Cell Dysfunction ◽  
Glutathione Redox Cycle ◽  
Tnf Α ◽  
Glutathione Redox
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