Muizelaar J P, van der Poel H G, Li Z C, Kontos H A, Levasseur J E
Division of Neurosurgery, Medical College of Virginia, Richmond.
J Neurosurg. 1988 Dec;69(6):923-7. doi: 10.3171/jns.1988.69.6.0923.
Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3- levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at a pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.
过度通气通过血管收缩可急性降低颅内压（ICP），但其对血管直径的长期影响尚不清楚。在7只3周前植入颅骨视窗的兔子中，研究了长时间过度通气对血管直径的影响。用戊巴比妥静脉滴注（1毫克/千克/小时）维持麻醉54小时。测量动脉血和脑池脑脊液（CSF）中的pH值、二氧化碳和碳酸氢根水平。用图像分割器测量31条软脑膜小动脉的直径。在进行基线测量后，将动脉血二氧化碳分压（pCO2）从38毫米汞柱降至25毫米汞柱，并每4小时让其恢复至38毫米汞柱并维持10分钟。最初血管收缩了13%，之后每4小时逐渐减少3%。因此，到第20小时，pCO2为25毫米汞柱时的血管直径已恢复到略高于pCO2为38毫米汞柱时的基线值。每4小时将pCO2暂时恢复到38毫米汞柱会引起血管舒张：4小时时为12%，到52小时逐渐增加至16%。因此，在52小时时，pCO2为25毫米汞柱时血管直径是基线的105%，pCO2为38毫米汞柱时增加到122%。动脉血pH值在20小时恢复到基线，脑脊液pH值在24小时恢复到基线。在整个实验过程中，血液和脑脊液中的碳酸氢根一直保持降低。在3次维持正常碳酸血症的对照实验中，同期血管直径、pH值和碳酸氢根水平均未改变。每4小时通过短暂过度通气测试的二氧化碳反应性也未改变。这些结果表明，过度通气在降低脑血容量方面的效果持续不到24小时，且仅应在实际ICP升高时使用。如果预防性使用，当ICP因其他原因开始升高时其效果可能已经消失，且无法进一步降低pCO2。此外，较低碳酸氢根导致缓冲能力下降，使血管对动脉血二氧化碳分压（PaCO2）变化更敏感。这可能导致在PaCO2短暂升高时，如头部受伤患者进行气管内吸痰时，ICP出现更明显的升高。
