Sex hormones affect bone marrow dysfunction after trauma and hemorrhagic shock

Area of Science:

• Physiology
• Hematology
• Endocrinology

Background:

• Trauma and hemorrhagic shock (T/HS) can lead to bone marrow (BM) dysfunction, impairing progenitor cell growth.
• This dysfunction is mediated by plasma factors and has primarily been studied in male animals.
• The role of sex hormones in post-T/HS BM dysfunction remains largely unexplored.

Purpose of the Study:

• To investigate the influence of sex hormones on bone marrow (BM) dysfunction following trauma and hemorrhagic shock (T/HS).
• To compare BM progenitor clonogenic growth in castrated male rats, ovariectomized female rats, and proestrus female rats after T/HS.

Main Methods:

• Laboratory experiment involving Sprague-Dawley rats (castrated males, ovariectomized females, proestrus females, and noncastrated males).
• Rats underwent either T/HS or sham shock.
• Bone marrow (BM) mononuclear cells and plasma were harvested 3 hours post-resuscitation.
• Clonogenic growth of BM progenitors (erythroid burst-forming unit and granulocyte-macrophage colony-forming unit) was assessed.

Main Results:

• Noncastrated male rats subjected to T/HS showed significantly reduced BM progenitor colony formation compared to sham groups and all T/HS-affected female/castrated male groups.
• Plasma from noncastrated shocked male rats suppressed BM progenitor growth in vitro.
• This plasma-mediated suppression was lost when using plasma from castrated male rats subjected to T/HS.

Conclusions:

• Profound BM dysfunction after T/HS in male rats is not observed in proestrus female rats or castrated male rats.
• Plasma-mediated BM suppression following T/HS is dependent on the presence of male sex hormones.
• Sex hormones play a critical role in modulating bone marrow dysfunction after trauma and hemorrhagic shock.