Kovách A G, Dóra E, Hamar J, Eke A, Szabó L
Adv Exp Med Biol. 1977;94:705-11. doi: 10.1007/978-1-4684-8890-6_97.
It has been shown by surface fluoro-reflectometry that stepwise decrease of arterial blood pressure causes a biphasic cerebrocortical vascular volume response. After the arterial blood pressure decrease the vascular volume first decreased and later increased. In both parts of the biphasic reflectance change, the cerebrocortical NAD-NADH redox state shifted considerably towards reduction and there was no reoxidation after the onset of cortical vasodilatation. Since a very rapid NADH reduction occurred during the first 30 secs. of the arterial hypotension in parallel with the vascular volume decrease, it is suggested that in the transient phase of arterial hypotension cerebral hypoxia may occur. Furthermore it is suggested that anaerobic tissue metabolites or some unknown NAD-NADH dependent process might dilate the cerebrocortical arterial network during the autoregulatory adjustment of CBF. The participation of the sympathetico-adrenal system in transient brain hypoxia caused by bleeding is a possibility since both the early vasoconstriction and the steep NADH reduction were prevented by the administration of phenoxybenzamine (1 mg/kg) before bleeding.
表面荧光反射测定法表明,动脉血压的逐步降低会引起双相性脑皮质血管容积反应。动脉血压降低后,血管容积先减小,随后增大。在双相反射率变化的两个阶段,脑皮质NAD - NADH氧化还原状态均显著向还原方向转变,且皮质血管扩张开始后无再氧化现象。由于在动脉低血压的最初30秒内NADH迅速还原,同时血管容积减小,提示在动脉低血压的短暂阶段可能会发生脑缺氧。此外,提示在脑血流量的自动调节过程中,无氧组织代谢产物或某些未知的NAD - NADH依赖性过程可能会使脑皮质动脉网络扩张。由于在出血前给予苯氧苄胺(1mg/kg)可预防早期血管收缩和NADH的急剧还原,因此交感 - 肾上腺系统可能参与了出血引起的短暂性脑缺氧。