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首页> 外文期刊>American Journal of Physiology >Dependence of acetylcholine and ADP dilation of pial arterioles on heme oxygenase after transfusion of cell-free polymeric hemoglobin.
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Dependence of acetylcholine and ADP dilation of pial arterioles on heme oxygenase after transfusion of cell-free polymeric hemoglobin.

机译：输注无细胞聚合血红蛋白后，乙酰胆碱和小动脉的ADP扩张对血红素加氧酶的依赖性。

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Polymers of cell-free hemoglobin have been designed for clinical use as oxygen carriers, but limited information is available regarding their effects on vascular regulation. We tested the hypothesis that the contribution of heme oxygenase (HO) to acetylcholine-evoked dilation of pial arterioles is upregulated 2 days after polymeric hemoglobin transfusion. Dilator responses to acetylcholine measured by intravital microscopy in anesthetized cats were blocked by superfusion of the HO inhibitor tin protoporphyrin-IX (SnPPIX) in a group that had undergone exchange transfusion with hemoglobin 2 days earlier but not in surgical sham and albumin-transfused groups. However, immunoblots from cortical brain homogenates did not reveal changes in expression of the inducible isoform HO1 or the constitutive isoform HO2 in the hemoglobin-transfused group. To test whether the inhibitory effect of SnPPIX was present acutely after hemoglobin transfusion, responses were measured within an hour of completion of the exchange transfusion. In control and albumin-transfused groups, acetylcholine responses were unaffected by SnPPIX but were blocked by addition of the nitric oxide synthase inhibitor N(omega)-nitro-l-arginine (l-NNA) to the superfusate. In hemoglobin-transfused groups, the acetylcholine response was blocked by either SnPPIX or l-NNA alone. The effect of another HO inhibitor, chromium mesoporphyrin (CrMP), was tested on ADP, another endothelial-dependent dilator, in anesthetized rats. Pial arteriolar dilation to ADP was unaffected by CrMP in controls but was attenuated 62% by CrMP in rats transfused with hemoglobin. It is concluded that 1) polymeric hemoglobin transfusion acutely upregulates the contribution of HO to acetylcholine-induced dilation of pial arterioles in cats, 2) this upregulation persists 2 days after transfusion when 95% of the hemoglobin is cleared from the circulation, and 3) this acute upregulation of HO signaling is ubiquitous in that similar effects were observed with a different endothelial-dependent agonist (i.e., ADP) in a another species (rat).
机译：无细胞血红蛋白的聚合物已被设计用于临床作为氧气载体，但关于其对血管调节作用的信息有限。我们测试了以下假设：在聚合物血红蛋白输注后2天，血红素加氧酶（HO）对乙酰胆碱引起的小动脉小动脉扩张的贡献被上调。在接受麻醉的猫中，通过活体显微镜测量的扩张剂对乙酰胆碱的反应被HO抑制剂锡原卟啉-IX（SnPPIX）的灌注所阻断，该组在2天前与血红蛋白进行了交换输血，但在手术假组和白蛋白输注组中没有。然而，来自皮质脑匀浆的免疫印迹未显示血红蛋白输注组中诱导型同工型HO1或组成型同工型HO2表达的变化。为了测试在血红蛋白输注后是否急性存在SnPPIX的抑制作用，在交换输血完成后一小时内测量反应。在对照组和输注白蛋白的组中，乙酰胆碱反应不受SnPPIX的影响，但通过向一熔液中添加一氧化氮合酶抑制剂N（ω）-硝基-1-精氨酸（1-NNA）来阻断。在输注血红蛋白的组中，单独的SnPPIX或1-NNA阻断了乙酰胆碱反应。在麻醉的大鼠中，对另一种依赖内皮的扩张剂ADP对另一种HO抑制剂铬中卟啉（CrMP）的作用进行了测试。在对照组中，CrMP不会影响小动脉向ADP的扩张，但在输注血红蛋白的大鼠中，CrMP会使其衰减62％。结论是：1）聚合性血红蛋白输注急性上调了HO对猫胆碱诱导的乙酰胆碱诱导的扩张的作用; 2）当输血后95％的血红蛋白清除后，这种上调在输血后2天持续存在。 HO信号转导的这种急性上调是普遍存在的，因为在另一物种（大鼠）中用不同的内皮依赖性激动剂（即ADP）观察到了相似的作用。

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