McCalden T A, Eidelman B H, Bloom D
Stroke. 1976 Mar-Apr;7(2):190-3. doi: 10.1161/01.str.7.2.190.
The cerebrovascular response to hypercapnia and hyperventilation was studied in normal and jaundiced baboons by the intracarotid 133Xe injection technique. The baboons with bile duct ligation were found to have decreased CBF at all levels of PaCO2. This difference between normal and jaundiced baboons was 13% at normocapnia rising to 33% with hypercapnia and 37% with hypocapnia. The CBF values all were increased toward normal by use of an alpha-adrenoreceptor blockade (phentolamine). It is suggested that the obstructive jaundice potentiated an inherent vasoconstrictor alpha-adrenergic mechanism to oppose the effects of CO2. Also, alteration of the PaCO2 may have produced its effects on the cerebral vessels by altering this adrenergic mechanism.
通过颈内注射¹³³Xe技术，研究了正常和黄疸狒狒对高碳酸血症和过度通气的脑血管反应。发现胆管结扎的狒狒在所有PaCO₂水平下脑血流量（CBF）均降低。正常狒狒和黄疸狒狒之间的这种差异在正常碳酸血症时为13%，高碳酸血症时升至33%，低碳酸血症时为37%。使用α-肾上腺素能受体阻滞剂（酚妥拉明）后，CBF值均向正常水平增加。提示梗阻性黄疸增强了固有的血管收缩性α-肾上腺素能机制，以对抗CO₂的作用。此外，PaCO₂的改变可能通过改变这种肾上腺素能机制而对脑血管产生影响。
