De Salles A A, Manchola I
Division of Neurosurgery, School of Medicine, University of California, Los Angeles.
J Neurosurg. 1994 Apr;80(4):624-30. doi: 10.3171/jns.1994.80.4.0624.
Arteriovenous malformations (AVM's) are congenital tangles of vessels that have a high blood flow through a low-resistance nidus. The vessels in the nidus may lack normal vasoreactivity in response to changes in PaCO2 or perfusion pressure (autoregulation). Arteriovenous malformation hemodynamics have been assessed based on the response of AVM feeding arteries to hypocapnia. Twenty-five AVM patients, aged 34 +/- 11 years (mean +/- standard deviation), were admitted to the Massachusetts General Hospital for proton-beam radiation therapy. Fourteen healthy volunteers aged 30 +/- 7 years served as control subjects. Angiograms with calibrated markers permitting magnification correction were available for all patients. The limits of the middle cerebral artery, as determined by transcranial Doppler ultrasonography, were compared to measurements made on the angiograms. Hyperventilation was induced at a rate set by a metronome. Fixed bilateral Doppler probes allowed almost simultaneous sampling of two vessels. Volunteer control subjects were hyperventilated in two steps. The two PaCO2 step decreases were significant (mean resting PaCO2 40.6 +/- 3.5 mm Hg, Step 1 level 29.4 +/- 3.5 mm Hg and Step 2 level 23.8 +/- 3.5 mm Hg; p < 0.01). These decreases induced a significant decrease in mean flow velocity (Vm) and an increase in the pulsatility index (p < 0.001). Mean carbon dioxide reactivity (% delta Vm/delta PaCO2) was 2.74 +/- 1.0 for Step 1 and 1.44 +/- 1.8 for Step 2 (p < 0.003). The mean PaCO2 decrease in patients was from 39.5 +/- 4.0 mm Hg to 27.0 +/- 3.5 mm Hg. Carbon dioxide reactivity was 0.92 +/- 1.12 for feeding vessels and 2.59 +/- 1.78 for nonfeeding vessels (p < 0.001). Transcranial Doppler ultrasound and angiographic depth measurements correlated well. Hyperventilation induced significantly more hemodynamic changes in control and nonfeeding middle cerebral arteries than in feeding vessels. Impaired CO2 reactivity may help to identify AVM feeding vessels as well as the relative magnitude of the flow provided to the malformation.
动静脉畸形（AVM）是先天性血管缠结，通过低阻力病灶有高血流量。病灶内的血管可能缺乏对动脉血二氧化碳分压（PaCO2）或灌注压变化的正常血管反应性（自动调节）。基于AVM供血动脉对低碳酸血症的反应评估了动静脉畸形血流动力学。25例年龄为34±11岁（平均±标准差）的AVM患者被收入马萨诸塞州总医院接受质子束放射治疗。14名年龄为30±7岁的健康志愿者作为对照受试者。所有患者均有带校准标记且可进行放大校正的血管造影照片。将经颅多普勒超声测定的大脑中动脉界限与血管造影照片上的测量结果进行比较。以节拍器设定的速率诱导过度通气。固定的双侧多普勒探头可几乎同时对两根血管进行采样。志愿者对照受试者分两步进行过度通气。两次动脉血二氧化碳分压（PaCO2）阶梯式降低均显著（平均静息PaCO2为40.6±3.5毫米汞柱，第一步水平为29.4±3.5毫米汞柱，第二步水平为23.8±3.5毫米汞柱；p<0.01）。这些降低导致平均流速（Vm）显著降低，搏动指数增加（p<0.001）。第一步的平均二氧化碳反应性（%ΔVm/ΔPaCO2）为2.74±1.0，第二步为1.44±1.8（p<0.003）。患者的平均PaCO2降低幅度为从39.5±4.0毫米汞柱降至27.0±3.5毫米汞柱。供血血管的二氧化碳反应性为0.92±1.12，非供血血管为2.59±1.78（p<0.001）。经颅多普勒超声和血管造影深度测量结果相关性良好。过度通气在对照和非供血大脑中动脉中诱导的血流动力学变化比在供血血管中显著更多。二氧化碳反应性受损可能有助于识别AVM供血血管以及向畸形提供的血流量的相对大小。
