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猫软脑膜小动脉二氧化碳作用的局部机制。

Local mechanism of CO2 action of cat pial arterioles.

作者信息

Kontos H A, Wei E P, Raper A J, Patterson J L

出版信息

Stroke. 1977 Mar-Apr;8(2):226-9. doi: 10.1161/01.str.8.2.226.

DOI:10.1161/01.str.8.2.226
PMID:15334
Abstract

The effect of local hypercapnic acidosis or local hypocapnic alkalosis on pial arterioles were studied in anesthetized cats equipped with a cranial window for the direct observation of the pial microcirculation of the parietal cortex. Changes in PCO2 and pH of the extracellular fluid were induced by perfusing the space under the cranial window with artificial cerebrospinal fluid equilibrated with different concentrations of CO2, while PaCO2 was maintained constant. Hypercapnic acidosis dilated and hypocapnic alkalosis constricted pial arteioles markedly. The results indicate that a basis exists for considering CO2 as a mediator for local regulation of brain blood flow. The vasodilation associated with arterial hypercapnia was abolished by a reduction in CSF PCO2 equal in magnitude to the rise in arterial blood PCO2, suggesting that the action of CO2 is entirely local.

摘要

在配备用于直接观察顶叶皮质软膜微循环的颅窗的麻醉猫中,研究了局部高碳酸血症酸中毒或局部低碳酸血症碱中毒对软膜小动脉的影响。通过用与不同浓度二氧化碳平衡的人工脑脊液灌注颅窗下的空间来诱导细胞外液中PCO2和pH的变化,同时将动脉血二氧化碳分压(PaCO2)维持恒定。高碳酸血症酸中毒使软膜小动脉明显扩张,低碳酸血症碱中毒使其明显收缩。结果表明,存在将二氧化碳视为脑血流局部调节介质的依据。与动脉高碳酸血症相关的血管舒张被脑脊液PCO2降低所消除,降低幅度与动脉血PCO2升高幅度相同,这表明二氧化碳的作用完全是局部性的。

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