Intravenous recombinant erythropoietin does not lead to an increase in cerebrospinal fluid erythropoietin concentration

Abstract

Many studies have shown a close link between erythropoietin (Epo) and the brain. Epo mRNA has been found in biopsies from the human hippocampus, amygdala and temporal cortex. Low levels of oxygen can lead to increased Epo mRNA levels in the monkey brain, similar to that found in the mouse brain during the state of anaemia [1]. Moreover, brain capillary endothelial cells express two forms of Epo mRNA receptor [2] and Epo receptors are found in the central nervous system of mid-trimester human fetuses [3]. Moreover, in vitro studies have shown that Epo has a neuroprotective effect and this can prevent neuronal death induced by glutamate in a dose-dependent manner [4]. Recent findings by Marti et al. [5] demonstrate that Epo can originate directly from the brain. In the absence of important lesions, Epo produced by the kidney does not cross the blood brain barrier (BBB) [5]. To our knowledge, it is not known whether i.v. recombinant human erythropoietin (rHuEpo) can modify cerebral flow parameters and the characteristics of cerebrospinal fluid (CSF).