Effect of local change in O2 saturation of hemoglobin on cerebral vasodilation from hypoxia and hypotension.
Effect of local change in O2 saturation of hemoglobin on cerebral vasodilation from hypoxia and hypotension.
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血红蛋白氧饱和度的局部变化对缺氧和低血压引起的脑血管舒张的影响。
DOI：
10.1152/ajpheart.1993.265.4.h1439
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Kontos,HA
中科院分区：
文献类型：
--
作者：
Wei,EP;Randad,RS;Levasseur,JE;Abraham,DJ;Kontos,HA
我们测试了某些新合成的血红蛋白变构调节剂对装有颅窗的麻醉猫脑小动脉因动脉缺氧、动脉低血压和动脉高碳酸血症引起的扩张的影响，以观察脑微循环。血红蛋白的变构调节剂是2-(芳氧基)-2-甲基丙酸的异构体。它们将血红蛋白的氧解离向右移动，从而促进氧气的局部释放。当这些化合物以 0.1 mM 的浓度以 1 ml/min 的速率局部灌注时，它们对基线动脉直径没有显着影响，但显着减少动脉缺氧和动脉低血压引起的血管舒张。它们不影响动脉高碳酸血症引起的血管舒张。对直径为 50-80 微米的软脑膜静脉的光密度进行分光光度测量表明，变构化合物的灌注降低了室内空气呼吸期间和缺氧期间的血红蛋白氧饱和度。我们的结论是，动脉缺氧和动脉低血压引起的血管舒张是由局部氧依赖性机制介导的。血红蛋白的变构调节剂可作为研究氧依赖性机制的有用工具。
We tested the effect of certain newly synthesized allosteric modifiers of hemoglobin on the dilation induced by arterial hypoxia, arterial hypotension, and arterial hypercapnia in cerebral arterioles of anesthetized cats equipped with cranial windows for the observation of the cerebral microcirculation. The allosteric modifiers of hemoglobin are isomers of 2-(aryloxy)-2-methylpropionic acid. They shift the oxygen dissociation of hemoglobin to the right, thereby facilitating the local release of oxygen. When these compounds were applied topically by superfusion at a rate of 1 ml/min in a concentration of 0.1 mM, they had no significant effect on baseline arteriolar diameter but reduced significantly the vasodilation from arterial hypoxia and arterial hypotension. They did not influence the vasodilation from arterial hypercapnia. Spectrophotometric measurements of optical densities from pial veins 50-80 microns in diameter indicated that the superfusion with the allosteric compounds reduced hemoglobin oxygen saturation both during room air breathing and during hypoxia. We conclude that the vasodilations from arterial hypoxia and arterial hypotension are mediated by local oxygen-dependent mechanisms. The allosteric modifiers of hemoglobin may be useful as tools in investigating oxygen-dependent mechanisms.