Kontos H A, Wei E P, Raper A J, Rosenblum W I, Navari R M, Patterson J L
Am J Physiol. 1978 May;234(5):H582-91. doi: 10.1152/ajpheart.1978.234.5.H582.
The mechanism of action of hypoxia on cerebral blood vessels and its role in the regulation of the cerebral circulation were investigated in anesthetized cats. Arterial hypoxia produced marked cerebral arteriolar vasodilation, which was partially reversed by perfusing the space under the cranial window with artificial cerebrospinal fluid (CSF) containing 6-94% oxygen. More marked increase in the local supply of oxygen, via perfusion of the space under the cranial window with fluorocarbon FC-80 equilibrated with 100% oxygen, completely eliminated the vasodilation induced by arterial hypoxia. Fluorocarbon equilibrated with 100% N2 had no effect on the vasodilation. The vasodilation associated with hypotension was completely reversed by perfusion with fluorocarbon equilibrated with 100% oxygen and was unaffected by perfusion with fluorocarbon or CSF equilibrated with gas not containing oxygen. The vasodilation associated with Metrazole-induced seizures was partially reversed by perfusion with fluorocarbon containing oxygen. The results show that hypoxia dilated cerebral blood vessels entirely via a local mechanism, that hypoxia is the dominant mechanism involved in the vasodilation associated with hypotension, and that it is, at least partially, responsible for the vasodilation associated with seizures.
在麻醉猫身上研究了缺氧对脑血管的作用机制及其在脑循环调节中的作用。动脉缺氧导致明显的脑小动脉血管舒张，通过向颅窗下间隙灌注含6 - 94%氧气的人工脑脊液（CSF），这种血管舒张可部分逆转。通过向颅窗下间隙灌注用100%氧气平衡的氟碳化合物FC - 80，使局部氧气供应更显著增加，完全消除了动脉缺氧诱导的血管舒张。用100%氮气平衡的氟碳化合物对血管舒张无影响。与低血压相关的血管舒张通过用100%氧气平衡的氟碳化合物灌注可完全逆转，而用不含氧气的气体平衡的氟碳化合物或CSF灌注对此无影响。与戊四氮诱发癫痫相关的血管舒张通过用含氧氟碳化合物灌注可部分逆转。结果表明，缺氧完全通过局部机制使脑血管舒张，缺氧是与低血压相关的血管舒张的主要机制，并且它至少部分地导致了与癫痫相关的血管舒张。
