Erythropoietin (EPO) is a potent cytoprotective cytokine that has been shown to reduce acute ischemia-reperfusion (I/R) injury in the brain, spinal cord, heart, liver and kidney independent of its hematopoietic effects. Although it may have other mechanisms of action, up-regulation of endothelial nitric oxide synthase (eNOS) and NO production by the vascular endothelium appears to be important. We tested whether human recombinant EPO (rhEPO) would protect against acute lung I/R injury of 90 min left hilar clamping followed by 4 hr of reperfusion in anesthetized Sprague-Dawley rats. Three groups of 5 rats were studied: a) CONT- thoracotomy but no I/R injury, b) I/R injury, and c) I/R injury plus 24 hr pretreatment with 5000 units/kg rhEPO. Gas exchange, hemodynamics, exhaled nitric oxide, and serum LDH were measured before and after 4 hr of reperfusion. Changes in lung wet to dry weight ratio and broncho-alveolar lavage fluid (BAL) protein, neutrophils (PMN) and tumor necrosis factor (TNF) were assessed. (Table)
EPO increased exhaled NO before the I/R protocol by almost 4-fold; 1.6 vs. 6.3 parts per billion (P ≤ 0.01). These findings of roughly 50-90% reduction in a variety of injury parameters demonstrate that EPO is effective in limiting acute lung I/R injury and that it may do so by increasing NO production.
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