Dóra E, Kovách A G
J Cereb Blood Flow Metab. 1982;2(2):209-19. doi: 10.1038/jcbfm.1982.21.
The effects of stepwise arterial hypotension (MABP: 80, 60, 40 mm Hg) and moderate arterial hypo- and hypertension (MABP: 80, 150-160 mm Hg) on cerebrocortical vascular volume and NAD/NADH redox state were studied in anaesthetized cats. The vascular volume and NADH fluorescence measurements were performed on closed skull preparations using a microscope fluororeflectometer. To determine the possible role of adrenergic alpha-receptors in the autoregulatory adjustment of cerebrocortical vascular volume, some of the animals were pretreated with intra-arterially infused phenoxybenzamine (1 mg/kg). It was found that longlasting stepwise arterial hypotension leads to a gradual increase in cerebrocortical vascular volume and NADH fluorescence. Though the cerebrocortical arteries dilatated considerably at 80 mm Hg, sustained for 30 min, the NAD/NADH redox state failed to be reoxidized but was shifted to a more reduced state. This finding suggests that some factor other than tissue hypoxia is responsible for the dilatation of cerebrocortical vessels during moderate arterial hypotension. When the arterial blood pressure was restored following stepwise arterial hypotension, the cerebrocortical vascular volume did not decrease and the NAD/NADH redox state remained reduced, showing that the autoregulatory capability of the vessels was lost and the tissue metabolism was irreversibly altered. During a 5-min duration of moderate arterial hypo- and hypertension, biphasic changes were obtained in cerebrocortical vascular volume while the NAD/NADH redox state was shifted to a more reduced and oxidized state. Since the dilatation and the constriction of the cerebrocortical vessels during arterial hypo- and hypertension lagged by 40-80 s behind the redox state alterations, it is suggested that the myogenic mechanism has a minor role in CBF autoregulation. Phenoxybenzamine (PBZ) dilatated the cerebrocortical vessels, indicating the existence of an active alpha-receptor-mediated vasoconstrictory tone. Since the extent of autoregulatory vascular volume changes was not affected by PBZ pretreatment, the involvement of adrenergic alpha-receptors in the autoregulation of CBF can be excluded, at least for cats.
在麻醉猫身上研究了逐步动脉低血压（平均动脉压：80、60、40 mmHg）以及中度动脉低血压和高血压（平均动脉压：80、150 - 160 mmHg）对大脑皮质血管容量和NAD/NADH氧化还原状态的影响。使用显微镜荧光反射计在闭合颅骨标本上进行血管容量和NADH荧光测量。为了确定肾上腺素能α受体在大脑皮质血管容量自动调节中的可能作用，部分动物经动脉内注入酚苄明（1 mg/kg）进行预处理。结果发现，持续性逐步动脉低血压会导致大脑皮质血管容量和NADH荧光逐渐增加。尽管大脑皮质动脉在80 mmHg时显著扩张并持续30分钟，但NAD/NADH氧化还原状态未能重新氧化，而是转变为更还原的状态。这一发现表明，在中度动脉低血压期间，除组织缺氧外的某些因素导致了大脑皮质血管的扩张。在逐步动脉低血压后恢复动脉血压时，大脑皮质血管容量并未减少，且NAD/NADH氧化还原状态仍保持还原，表明血管的自动调节能力丧失，组织代谢发生了不可逆改变。在中度动脉低血压和高血压持续5分钟期间，大脑皮质血管容量出现双相变化，而NAD/NADH氧化还原状态转变为更还原和氧化的状态。由于在动脉低血压和高血压期间大脑皮质血管的扩张和收缩比氧化还原状态改变滞后40 - 80秒，提示肌源性机制在脑血流量自动调节中作用较小。酚苄明（PBZ）使大脑皮质血管扩张，表明存在活跃的α受体介导的血管收缩张力。由于自动调节的血管容量变化程度不受PBZ预处理的影响，至少对于猫而言，可以排除肾上腺素能α受体参与脑血流量的自动调节。
