Strauss G, Hansen B A, Knudsen G M, Larsen F S
Department of Hepatology, Rigshospitalet, University Hospital, Copenhagen, Denmark.
J Hepatol. 1998 Feb;28(2):199-203. doi: 10.1016/0168-8278(88)80006-0.
BACKGROUND/AIMS: In patients with acute liver failure loss of cerebral blood flow autoregulation may result from cerebral vasodilatation. Since arterial hypocapnia induces cerebral vasoconstriction, we investigated whether cerebral blood flow autoregulation could be reestablished by mechanical hyperventilation.
Seven consecutive patients (median age 45, range 30-50 years) with acute liver failure and hepatic encephalopathy stage IV entered the study. They were all maintained on mechanical ventilation. Cerebral blood flow autoregulation was evaluated by using transcranial Doppler sonography to assess mean flow velocity (Vmean) in the middle cerebral artery, during a rise in mean arterial pressure by norepinephrine infusion (0.5-10 microg/h). The patients were subsequently hyperventilated for 15 min before cerebral blood flow autoregulation was re-evaluated in the same mean arterial pressure range.
At baseline PaCO2 (4.0 (3.5-4.9)kPa), all patients had impaired cerebral blood flow autoregulation as Vmean increased from 47 (30-78) to 68 (49-107) cm x s(-1) (p<0.05), as MAP was raised from 82 (60-88) to 106 (89-123) mmHg. During hyperventilation, five of seven patients restored cerebral autoregulation as Vmean remained unchanged at 51 (45-70) cm x s(-1) during a rise in MAP from 84 (65-94) to 110 (89-130) mmHg. Cerebral blood flow autoregulation was not restored in two patients, but hyperventilation reduced the slope of the mean arterial pressure-Vmean correlation. These two patients had renal failure and were treated with intermittent hemodialysis.
Cerebral blood flow autoregulation was restored by hyperventilation in five of seven patients with acute liver failure, indicating that cerebral vasodilatation is of pathophysiological importance in dysregulation of cerebral circulation in acute liver failure.
背景/目的：在急性肝衰竭患者中，脑血流自动调节功能丧失可能是由脑血管扩张引起的。由于动脉低碳酸血症会诱发脑血管收缩，我们研究了机械性过度通气是否能重建脑血流自动调节功能。
连续7例急性肝衰竭且处于肝性脑病IV期的患者（中位年龄45岁，范围30 - 50岁）进入本研究。他们均接受机械通气。通过经颅多普勒超声评估大脑中动脉的平均血流速度（Vmean）来评价脑血流自动调节功能，期间通过输注去甲肾上腺素（0.5 - 10微克/小时）使平均动脉压升高。随后患者进行15分钟的过度通气，之后在相同的平均动脉压范围内重新评估脑血流自动调节功能。
在基线时，动脉血二氧化碳分压（PaCO2）为4.0（3.5 - 4.9）千帕，所有患者的脑血流自动调节功能均受损，随着平均动脉压从82（60 - 88）毫米汞柱升至106（89 - 123）毫米汞柱，Vmean从47（30 - 78）厘米/秒增加至68（49 - 107）厘米/秒（p<0.05）。在过度通气期间，7例患者中有5例恢复了脑自动调节功能，当平均动脉压从84（65 - 94）毫米汞柱升至110（89 - 130）毫米汞柱时，Vmean保持在51（45 - 70）厘米/秒不变。2例患者的脑血流自动调节功能未恢复，但过度通气降低了平均动脉压与Vmean相关性的斜率。这2例患者患有肾衰竭并接受间歇性血液透析治疗。
7例急性肝衰竭患者中有5例通过过度通气恢复了脑血流自动调节功能，表明脑血管扩张在急性肝衰竭脑循环调节异常中具有病理生理学重要性。
