Sex hormones affect bone marrow dysfunction after trauma and hemorrhagic shock.
OBJECTIVE
Bone marrow (BM) dysfunction after trauma and hemorrhagic shock (T/HS) results in a decrease in clonogenic growth of BM progenitors through a plasma-mediated process. Although sex hormones have been shown to modulate some end-organ injury after shock, post-T/HS BM dysfunction has only been studied in male animals. Therefore, the present study examines the effects of sex hormones on post-T/HS BM dysfunction by measuring clonogenic growth of BM progenitors in castrated male rats and in ovariectomized and proestrus female rats.


METHODS
Laboratory experiment.


METHODS
University surgical research laboratory.


METHODS
Castrated and noncastrated male and ovariectomized and proestrus female Sprague-Dawley rats.


METHODS
All rats were subjected to either T/HS or sham shock with laparotomy (n = 3-5 per group). At 3 hrs after resuscitation, the rats were killed and plasma and BM mononuclear cells from bilateral femurs were harvested.


RESULTS
BM mononuclear cells were cultured for erythroid burst-forming unit and granulocyte-macrophage colony-forming unit colonies to assess the extent of progenitor BM dysfunction. BM from noncastrated male rats subjected to T/HS demonstrated a significant decrease in granulocyte-macrophage colony-forming unit and erythroid burst-forming unit colony formation compared with BM of all the sham shock groups and with the castrated male and both female rat groups subjected to T/HS. In addition, plasma from noncastrated shocked male rats incubated in vitro with BM cells from unmanipulated male rats caused a significant suppression of BM granulocyte-macrophage colony-forming unit and erythroid burst-forming unit colonies compared with plasma from castrated rats subjected to either sham shock with laparotomy or T/HS.


CONCLUSIONS
The profound BM dysfunction observed in noncastrated male rats after T/HS is not observed in proestrus female rats and castrated male rats. In addition, the in vitro plasma-mediated BM suppression present in male rats after T/HS is also lost in castrated male rats. Sex hormones seem to play a significant role in BM dysfunction after T/HS.
Sifri
Ziad C
ZC
Division of Trauma, Department of Surgery, New Jersey Medical School, Newark, NJ, USA.
Cohen
David
D
Ananthakrishnan
Preya
P
Wang
Lai
L
Kaiser
Vicki L
VL
Mohr
Alicia M
AM
Hauser
Carl J
CJ
Rameshwar
Pranela
P
Deitch
Edwin A
EA
Livingston
David H
DH
D000818:Animals; D001853:Bone Marrow / Q000503:physiopathology*; D003114:Colony-Forming Units Assay; D015672:Erythroid Precursor Cells / Q000502:physiology; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D042381:Granulocyte Precursor Cells / Q000502:physiology; D006412:Hematopoietic Stem Cells / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D008297:Male; D009919:Orchiectomy; D010052:Ovariectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D014947:Wounds and Injuries / Q000503:physiopathology*
D012739:Gonadal Steroid Hormones