Anemia increases the risk of renal cortical and medullary hypoxia during cardiopulmonary bypass
Anemia increases the risk of renal cortical and medullary hypoxia during cardiopulmonary bypass
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DOI：
10.1177/0267659113490219
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发表时间：
2013-11-01
期刊：
影响因子：
1.2
通讯作者：
Mazer, C. D.
中科院分区：
文献类型：
--
作者：
Darby, P. J.;Kim, N.;Mazer, C. D.
简介：贫血是体外循环(CPB)后急性肾损伤(AKI)的独立预测因子，可能是由于肾脏供氧不足所致。本研究旨在探讨体外循环和贫血对肾皮质和髓质组织氧分压(PO2)和血流量的影响。方法：大鼠(n=6)常温体外循环(CPB)1h，目标血红蛋白浓度(Hb)分别为10g/dL(CPB)和6.5g/dL(贫血-CPB)。测定CPB前、中、后1h肾血流量(RBF)和组织氧分压(PO2)。为了证实肾皮质和髓质PO2的差异，将HIF-1α(ODD)荧光素酶小鼠暴露于8%O-2(低氧)中，并在肾皮质和髓质(n=5)测量HIF-1α依赖的发光。结果：肾组织PO2在CPB开始时下降，并恢复到基线水平，但在CPB结束时，PO2值恢复到基线水平。贫血-CPB导致肾皮质和髓质血流量显著增加，PO2在整个贫血-CPB期间保持显著降低。肾髓质缺氧诱导因子-1α依赖的发光证实了肾髓质中更严重的缺氧。讨论：在体外循环期间，肾氧输送受到一过性损害，但在1小时后恢复。贫血-CPB导致肾皮质和髓质PO2显著和持续下降，这表明肾缺氧性损伤合并贫血的风险增加。结论：肾皮质和髓质缺氧程度的明显差异可能有助于了解CPB期间肾皮质和髓质缺氧的进展情况和AKI的潜在发展。进一步的研究应着眼于确定髓质缺氧的早期标志物和潜在的药物，这些药物可能会减少肾髓质的做功和氧耗，以减少CPB期间缺氧损伤和贫血的风险。
Introduction: Anemia is an independent predictor of acute kidney injury (AKI) following cardiopulmonary bypass (CPB), possibly due to inadequate renal oxygen delivery. The objective of this study was to investigate the effects of CPB and anemia on tissue oxygen tension (pO2) and blood flow in the renal cortex and medulla.Methods: Rats (n=6/group) underwent 1hr of normothermic cardiopulmonary bypass (CPB), with target hemoglobin concentrations (Hb) of 10g/dL (CPB) or 6.5g/dL (anemia-CPB). Renal blood flow (RBF) and tissue PO2 were measured before, during and after 1hr of CPB. To confirm the observed differences in renal cortical and medullary PO2, HIF-1 alpha (ODD) luciferase mice were exposed to 8% O-2 (hypoxia) and HIF-1 alpha dependent luminescence was measured in the renal cortex and medulla (n= 5).Results: Renal tissue PO2 values decreased initially and returned towards baseline, however, values at the end of CPB. Anemia-CPB resulted in a significant increase in both renal cortical and medullary blood flow, PO2 remained significantly reduced throughout anemia-CPB. Renal medullary HIF-1 alpha-dependent luminescence confirmed a greater degree of hypoxia in the renal medulla.Discussion: During CPB, renal O-2 delivery was transiently jeopardized, but recovered after 1hr. Anemia-CPB resulted in a dramatic and sustained reduction in renal cortical and medullary PO2, which suggests an increased risk of renal hypoxic injury with anemia.Conclusion: The clear difference in the degree of hypoxia in the renal cortex and medulla may be useful in understanding the progress of medullary hypoxia during CPB with anemia and the potential development of AKI. Further studies should aim at identifying early markers of medullary hypoxia and potential agents that may decrease the work and O-2 consumption in the renal medulla to reduce the risk of hypoxic damage during CPB and anemia.