Journal
SHOCK
Volume 31, Issue 3, Pages 227-237Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/SHK.0b013e31818347e7
Keywords
Sex; shock; estrogen receptors; androgen receptors
Funding
- National Institutes of Health [R37 GM39519, R01 GM37127]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM039519, R37GM039519, R01GM037127] Funding Source: NIH RePORTER
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Sex is increasingly recognized as a major factor in the outcome of patients who have trauma and sepsis. Moreover, sex steroids influence chemokine/adhesion molecule expression and neutrophil accumulation. Heat shock proteins, heat shock factor 1, and peroxisome proliferator-activated receptor gamma coactivator 1 are regulated by the estrogen receptors and consequently contribute to organ protection after trauma-hemorrhage. Additionally, sex steroids regulate inflammatory cytokines, leading to increased morbidity and mortality. This article deals with trauma-hemorrhage and examines the following: 1) the evidence for sex differences; 2) the mechanisms by which sex hormones affect organ protection; 3) the tissue-specific effect of sex hormone receptors; and 4) the effect of genomic and nongenomic (i.e. membrane-initiated steroid signaling) pathways of sex hormones after trauma. The available information indicates that sex steroids modulate cardiovascular responses after trauma. Thus, alteration or modulation of the prevailing hormone milieu at the time of injury seems to be a novel therapeutic option for improving outcome after injury.
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