Erythropoietin a safe bet in haemorrhagic shock?

IN this issue, Robinson et al. (1) present experimental
evidence for ineffective erythropoiesis in
a mouse model of haemorrhagic shock. What is the
rationale behind the observation of loss of erythropoietic
progenitors and enhanced apoptotic activity
in the bone marrow cells after haemorrhagic shock?
The authors indicate several possibilities, including
an immediate surge of tumour necrosis factor
(TNF)-a in circulation. Bleeding and replenishment
of the blood volume is believed to be a classical
physiological mechanism where lack of perfusion
volume causes hypoxia, followed by erythropoietin
secretion from the kidneys and blocked cell death
in erythroid progenitors resulting, in an increased
number of erythrocytes released into the circulation.
Robinson et al. may provide the first glimpse
of a more complex array of physiological responses
to haemorrhagic shock involving inflammation,
leading to ineffective erythropoiesis.