Effect of cross-linked hemoglobin transfusion on endothelial-dependent dilation in cat pial arterioles
Effect of cross-linked hemoglobin transfusion on endothelial-dependent dilation in cat pial arterioles
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DOI：
10.1152/ajpheart.1998.275.4.h1313
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发表时间：
1998-10-01
影响因子：
4.8
通讯作者：
Bucci, E
中科院分区：
文献类型：
--
作者：
Asano, Y;Koehler, RC;Bucci, E
我们确定了血浆中添加血红蛋白是否会抑制大脑中紧密内皮连接限制血红蛋白外渗的内皮依赖性扩张。在未输血（红细胞压积= 32%）或与白蛋白或癸二酸交联人血红蛋白溶液（红细胞压积= 18%）交换输血后，通过关闭的颅窗，通过活体显微镜测量麻醉猫的软脑膜小动脉直径。小、中、大动脉对乙酰胆碱和ADP的扩张作用不受血红蛋白输注的影响。的扩张反应被抑制的一氧化氮合酶抑制剂NG-硝基-L-精氨酸，虽然显着的扩张至30 μ M乙酰胆碱持续在小动脉中的控制和白蛋白输注组，但不是在血红蛋白输注组。对一氧化氮供体3-morpholinosynonimine的舒张反应不受白蛋白或血红蛋白输注的影响，但对硝普钠的反应在血红蛋白输注后减少了三分之一。当通过颅窗灌注交联血红蛋白时，乙酰胆碱反应在血红蛋白浓度为0.1 μ M时被抑制，在10 μ M时被完全阻断。由于该浓度基本上低于输血后血浆中500 μ M的血红蛋白浓度，此时不存在对乙酰胆碱反应的抑制，因此认为血红蛋白对血脑屏障的渗透可以忽略不计。我们的结论是，交换红细胞为基础的血红蛋白与血浆为基础的血红蛋白不产生更有效的汇内皮源性一氧化氮诱发激动剂受体介导的激活。此外，红细胞压积下降并不影响激动剂诱发的内皮依赖性扩张。
We determined whether addition of hemoglobin to the plasma would inhibit endothelial-dependent dilation in brain where tight endothelial junctions limit hemoglobin extravasation. Pial arteriolar diameter was measured by intravital microscopy through closed cranial windows in anesthetized cats either without transfusion (hematocrit = 32%) or after exchange transfusion with an albumin or sebacyl-cross-linked human hemoglobin solution (hematocrit = 18%). Dilation of small, medium, and large arterioles to acetylcholine and ADP was not significantly altered by hemoglobin transfusion. The dilatory responses were inhibited by the nitric oxide synthase inhibitor NG-nitro-L-arginine, although significant dilation to 30 mu M acetylcholine persisted in small arterioles in the control and albumin-transfused group but not in the hemoglobin-transfused group. The dilatory response to the nitric oxide donor 3-morpholinosydnonimine was unaffected by albumin or hemoglobin transfusion, but the response to nitroprusside was reduced by one-third after hemoglobin transfusion. When cross-linked hemoglobin was superfused through the cranial window, the acetylcholine response became inhibited at a hemoglobin concentration of 0.1 mu M and was completely blocked at 10 mu M. Because this concentration is substantially less than the 500 mu M hemoglobin concentration in plasma after transfusion when there was no inhibition of the acetylcholine response, hemoglobin permeation of the blood-brain barrier was considered negligible. We conclude that exchange of red cell-based hemoglobin with plasma-based hemoglobin does not produce a more effective sink for endothelial-derived nitric oxide evoked by agonist receptor-mediated activation. Furthermore, decreased hematocrit does not affect agonist-evoked endothelial-dependent dilation.