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.