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EPO Administration (epo + administration)
Selected AbstractsAnaemia in heart failure: a common interaction with renal insufficiency called the cardio-renal anaemia syndromeINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2 2008A. Palazzuoli Summary Background:, Although many studies have found a high prevalence of anaemia in patients with congestive heart failure (CHF), few have carefully examined the relationship between the CHF and the prevalence of anaemia and chronic renal insufficiency (CRI). Patients with advanced renal failure, significant anaemia, diffuse atherosclerosis, respiratory disease and more elderly patients have been systematically excluded from the great majority of the randomised clinical trials. Discussion:, Both anaemia and renal insufficiency are very common associated diseases associated with increased mortality, morbidity and rate of hospitalisation in CHF patients. Impaired renal function is associated with adverse outcomes because it represents a marker of coexistent disease and more diffuse atherosclerosis. In patients with CHF, progressive renal dysfunction leads to a decrease in erythropoietin (EPO) levels with reduced erythrocyte production from bone marrow. This may explain the common association between CHF, anaemia and CRI in clinical practice. The normalisation of haemoglobin concentration by EPO in patients with CHF and CRI results in improved exercise capacity by increasing oxygen delivery and improving cardiac function. Conclusion:, In this review, we describe the mechanisms linking anaemic status, CRI and CHF, the prognostic relevance of each disease, treatment implications, and potential benefit of EPO administration. [source] Erythropoietin attenuates white matter damage, proinflammatory cytokine and chemokine induction in developing rat brain after intra-uterine infectionNEUROPATHOLOGY, Issue 5 2009Ying Shen To investigate the possible ameliorating effect of recombinant human erythropoietin (rhEPO) on white matter damage, pro-inflammatory cytokine and chemokine induction in developing rat brain after intra-uterine Escherichia coli infection. E. coli was inoculated into uterine cervix of the time-pregnant rats and the control was injected with normal saline. Following maternal E. coli inoculation, the pups received a single intraperitoneal injection of rhEPO at a dose of 5000 IU/kg body weight immediately after birth. Immunohistochemical staining and Western blot analysis for 2,, 3,-cyclic nucleotide 3,-phosphodiesterase (CNPase), neurofilament (NF) and glial fibrillary acidic protein (GFAP) were performed to assess white matter damage in pup brains at post-natal day 1 (P1), P3 and P7. Pro-inflammatory cytokines and chemokines were detected by real-time quantitative RT-PCR at the mRNA levels to evaluate the inflammatory response in pup brains at P1, P3 and P7. A single dose of rhEPO treatment (5000 IU/kg body weight) attenuated white matter damage in developing rat brain after intra-uterine E. coli infection. The protein levels of CNPase and NF in pup brains at P7 significantly increased after post-natal rhEPO treatment as compared with the intra-uterine E. coli -treated group. Also, post-natal rhEPO injection markedly attenuated the intra-uterine E. coli infection-induced increases in GFAP protein expression and the mRNA levels of pro-inflammatory cytokines and chemokines. Post-natal EPO administration as a single dose may exert a neuroprotective effect on white matter damage by reducing pro-inflammatory cytokine and chemokine induction in developing rat brain after intra-uterine E. coli infection. [source] A novel endogenous erythropoietin mediated pathway prevents axonal degenerationANNALS OF NEUROLOGY, Issue 6 2004Sanjay C. Keswani MRCP Clinically relevant peripheral neuropathies (such as diabetic and human immunodeficiency virus sensory neuropathies) are characterized by distal axonal degeneration, rather than neuronal death. Here, we describe a novel, endogenous pathway that prevents axonal degeneration. We show that in response to axonal injury, periaxonal Schwann cells release erythropoietin (EPO), which via EPO receptor binding on neurons, prevents axonal degeneration. We demonstrate that the relevant axonal injury signal that stimulates EPO production from surrounding glial cells is nitric oxide. In addition, we show that this endogenous pathway can be therapeutically exploited by administering exogenous EPO. In an animal model of distal axonopathy, systemic EPO administration prevents axonal degeneration, and this is associated with a reduction in limb weakness and neuropathic pain behavior. Our in vivo and in vitro data suggest that EPO prevents axonal degeneration and therefore may be therapeutically useful in a wide variety of human neurological diseases characterized by axonopathy. Ann Neurol 2004 [source] The effects of sub-conjunctival EPO administration on ERG and on the peripheral blood haematocrit in animal model (rabbit)ACTA OPHTHALMOLOGICA, Issue 2009E DELGADO Purpose To assess the effects of subconjunctival EPO administration on retinal eletrophysiology and on the peripheral blood haematocrit. Methods New Zealand White rabbits (n=6) received 100 UI of EPO through the subconjuntival route. Blood for Complete Blood Count (CBC) was collected on day 0, on day 7 and on day 14 of the experimental protocol. Furthermore electroretinograms were performed on day 0 and on day 30 of the experiments. Results Regarding CBC changes, the haematocrit values changed from 35,42±2,7% on day 0 to 34,32±4,3% (p=0,390) on day 7 and to 34,45±4,4% on day 14 (p=0,931), showing no significant changes. Concerning the red blood cells (RBC x10000/µL) count, the values evolved from 6,02±0,48 on day 0 to 5,65±0,67 (p=0,074) on day 7 and to 5,67±0,74 (p=0,948) on day 14, showing no significant alterations. On the contrary, on what regards the electroretinograms, although there were no significant changes on a-wave amplitudes, which evolved from 13,94±1,7 µV on day 0 to 13,67±0,8 µV on day 30 (p=0,844) and no significant differences on N1-P1 amplitudes which changed from 46,60±4,5µV to 55,48±10,5 µV (p=0,438), there was a remarkable increase on b-wave amplitude of 49%, changing from 46,60±7,43 µV to 94,97±13,36 µV (p=0,031). Conclusion On what concerns CBC profiles, subconjuntival EPO administration did not cause any sinificant changes on haematocrit or RBC values. Regarding electrorretinography, there were no significant changes on a-wave or N1-P1 amplitudes, but there was a marked increase in the b-wave amplitude which tests for photoreceptor functionality, which might indicate a protective action against apoptosis of retinal photoreceptors even in physiological conditions. [source] Epo protects SOD2-deficient mouse astrocytes from damage by oxidative stressGLIA, Issue 4 2006Jing Liu Abstract Erythropoietin (Epo) expression, which regulates erythropoiesis, has been shown in rat and mouse brain after hypoxia. A previous study from our laboratory showed that astrocytes from manganese-superoxide dismutase (SOD2) homozygous knockout (SOD2,/,) mice can survive under 5% O2, but not under normal aerobic conditions. However, the mechanism involved is not clear. Our preliminary study using reverse transcriptase-polymerase chain reaction showed increased Epo mRNA expression in astrocytes cultured with 5% hypoxia compared with astrocytes under normal conditions. After administration of anti-sense Epo, protection decreased with time. Dose-dependent administration of Epo to SOD2,/, mouse astrocytes improved their survivability under normal conditions. Survivability of heterozygous SOD2,/+ mutant and wild-type mouse astrocyte cultures was the same under normal conditions but, after administration of 2 mM of paraquat, a reactive oxygen species generator, survivability of the SOD2,/+ astrocytes decreased remarkably compared with the wild-type cells. Epo administration 24 h before exposure to paraquat significantly improved the survivability of the SOD2,/+ astrocytes. Western blot studies suggest that Jak-Stat signal transduction pathways are involved in this process. Our study demonstrates an important role for Epo in the protection of astrocytes from reactive oxygen species. We suggest that Epo can compensate in part for the antioxidant properties of mitochondrial SOD2 deficiency. © 2005 Wiley-Liss, Inc. [source] | ||||||||||