异氟醚麻醉期间低碳酸血症和脑自主调节功能对脑血管阻力和表观零流压的影响

背景同步监测动脉血压（arterial blood pressure，ABP）和大脑中动脉血流速度可用于计算表观零流压（apparent zero flow pressure，aZFP）。压力一流速关系斜率的倒数被称为阻力面积乘积（resistance area product，RAP），是一项脑血管阻力指标。关于血管活性药物，动脉血二氧化碳分压（PaCO，）和脑自动调节功能受损在全身麻醉时对aZFP和RAP影响的研究很少。我们研究了异氟醚麻醉期间低碳酸血症和输注去氧肾上腺素对aZFP和RAP的影响。方法记录11名成年受试者在异氟醚麻醉期间桡动脉有创ABP和经颅多普勒所测的大脑中动脉血流速度信号。输注去氧肾上腺素增加ABP，调整通气以控制PaCO2。分别在两个不同的平均ABP水平（大约在80mmHg和100mmHg）和PaCO2水平（正常PaCO2：38～43mmHg和低碳酸水平：27～34mmHg），比较脑血流动力学的变化。对两种aZFP分析方法进行比较：一种基于线性回归，一种基于波形的傅立叶分析。结果在较低ABP水平，血碳酸正常时，aZFP为23±11mmHg，RAP为0．76±0．97mmHg·s·cm^-1；低碳酸血症时，aZFP为30±13mmHg（均数±标准差），RAP为1．16±0．16mmHg·s·cm^-1。，P〈0．001。在较高ABP水平可见到低碳酸血症带来的类似效应。血碳酸水平正常时，异氟醚对脑自主调节功能的损害及aZFP的影响不随ABP的上升而改变。低碳酸血症时，脑血管自动调节功能无明显损害，ABP的升高会使aZFP增加（从30±13mmHg增加到35±13mmHg，P〈0．01）和RAP增加（从1．16±0．16mmHg增加到1．52±0．20mmHg·S·cm^-1，P〈0．001）。评估aZFP和RAP对脑血流动力学的相对作用显示，RAP的变化显然比aZFP的变化在其中起更重要的作用。两种分析aZFP的方法（傅里叶分析法一线性回归法）的平均差为0．5±3．6mmHg（均数±2标准差）。结论异氟醚麻醉期间，低碳酸血症和大脑对ABP升高的自主调节反应，这两个因素可增加大脑小动脉张力，与RAP和aZFP的升高相关。RAP的变化显然比aZFP的变化产生更大的影响。这些结果提示小动脉张力通过控制血管阻力和有效灌注压来影响脑血流。

BACKGROUND： Simultaneous recordings of arterial blood pressure （ABP） and middle cerebral artery blood velocity can be used to calculate the apparent zero flow pressure （aZFP）. The inverse of the slope of the pressurevelocity relationship is known as resistance area product （RAP） and is an index of cerebrovascular resistance. There is little information available regarding the effects of vasoactive drugs, arterial carbon dioxide （PaCO2）, and impaired cerebral autoregulation on aZFP and RAP during general anesthesia. During isoflurane anesthesia, we investigated the effects of hypocapnia and the effects of a phenylephrine infusion, on aZFP and RAP. METHODS： Radial ABP and transcranial Doppler middle cerebral artery blood velocity signals were recorded in 11 adults undergoing isoflurane anesthesia. A phenylephrine infusion was used to increase ABP and ventilation was adjusted to control PaCO2. Cerebral hemodynamic variables were compared at two levels of mean ABP （approximately 80 and 100 mm Hg） and at two levels of PaCO2： normocapnia （PaCO2 38 -43 mm Hg） and hypocapnia （PaCO2 27 -34 mm Hg）. Two aZFP analysis methods were compared： one based on linear regression and one based on Fourier analysis of the waveforms. RESULTS： At the lowerABP, aZFP was 23 ± 11 mm Hg and 30 ± 13 mm Hg （mean ± SD） with normocapnia and hypocapnia, respectively （P 〈0.001） and RAP was 0.76 ± 0.97 mmHg·s·cm^-1 and 1.16 ± 0.16mmHg·s·cm^-1 with normocapnia and hypocapnia, respectively （P 〈 0. 001 ）. Similar effects of hypocapnia were seen at the higher ABP. With normocapnia, isoflurane impaired cerebral autoregulation and aZFP did nOt change with the increase in ABP. With hypocapnia, cerebral autoregulation was not significantly impaired and increasing ABP was associated with increasedaZFP （from 30 ± 13 to 35 ± 13 mmHg, P 〈 0. 01） and increased RAP （from 1.16 ± 0.16to 1.52 ± 0.20mmHg·s·cm^-1,P 〈 0. 001 ）. Calculation of the relative contributions of aZFP and RAP to the cerebral hemodynamic responses indicated that changes in RAP appeared to have a greater influence than changes in aZFP. The mean difference between the two methods of determining aZFP （Fourier-regression） was 0.5 ± 3.6 mm Hg （mean ± 2SD）. CONCLUSIONS： During isoflurane anesthesia, two interventions that increase cerebral arteriolar tone, hypocapnia and the autoregulatory response to increasing ABP, were associated with increased RAP and increased aZFP. The effect of changes in RAP appeared to be quantitatively greater than the effects of changes in aZFP. These results imply that arteriolar tone influences cerebral blood flow by controlling both resistance and effective downstream pressure.