Department of Neurology, Lucerne Kantonsspital, Spitalstrasse, CH-6000, Lucerne, Switzerland.
Department of Radiology, Section Neuroradiology, Lucerne Kantonsspital, Spitalstrasse, CH-6000, Lucerne, Switzerland.
Sci Rep. 2020 Jun 8;10(1):9213. doi: 10.1038/s41598-020-66317-x.
The mechanisms of high blood pressure (HBP) -related brain pathology progression remain relatively unclear. We investigated whether lowering BP in chronic HBP patients normalizes cerebral perfusion dynamics at resistance vessel and capillary levels. Sixty-seven patients with HBP and 49 age- and sex-matched healthy controls underwent simultaneous recordings of middle cerebral artery blood flow velocity (CBFV), BP, and end-tidal CO concentration. Thirty-four controls and 28 patients underwent additional near-infrared spectroscopy recordings (oxygenated [OHb] and deoxygenated [HHb] hemoglobin). Degree of microcirculatory white matter lesions was graded by Fazekas scale. Dynamic cerebral autoregulation (dCA) was assessed by transfer function analysis. BP was successfully lowered (patients = 89 ± 15 mm Hg, controls = 87 ± 17), but cerebrovascular resistance was higher in BP patients (p < 0.05). BP-CBFV phase was lower in very low frequency (VLF) (left/right: 48 ± 20°/44 ± 17; controls: 61 ± 20/60 ± 21; p < 0.001) and low frequency (LF) (34 ± 14/35 ± 14; controls: 48 ± 20/44 ± 17; p < 0.05) ranges. Gain was higher in VLF range (in %/ mm Hg 0.56 ± 0.44/0.59 ± 0.49; controls: 0.32 ± 0.29/0.34 ± 0.32; p ≤ 0.005). BP-CBFV phase and gain did not differ across Fazekas groups. Across all patients, the capillary phases and gains (CBFV-[O2Hb], CBFV-[HHb]) were comparable to controls. Successfully treated chronic HBP results in normal brain capillary hemodynamics while the resistance vessel state is disturbed (phase decrease, gain increase).
高血压(HBP)相关脑病理进展的机制尚不清楚。我们研究了降低慢性 HBP 患者的血压是否能使阻力血管和毛细血管水平的脑灌注动力学正常化。67 名 HBP 患者和 49 名年龄和性别匹配的健康对照者同时记录大脑中动脉血流速度(CBFV)、血压和呼气末 CO 浓度。34 名对照者和 28 名患者接受了近红外光谱记录(氧合[OHb]和去氧[HHb]血红蛋白)。通过 Fazekas 量表对微血管白质病变的程度进行分级。通过传递函数分析评估动态脑自动调节(dCA)。血压成功降低(患者=89±15mmHg,对照组=87±17mmHg),但脑血管阻力在高血压患者中较高(p<0.05)。BP-CBFV 相位在极低频率(VLF)(左/右:48±20°/44±17;对照组:61±20/60±21;p<0.001)和低频率(LF)(34±14/35±14;对照组:48±20/44±17;p<0.05)范围内较低。VLF 范围内的增益较高(以%/mmHg 表示,0.56±0.44/0.59±0.49;对照组:0.32±0.29/0.34±0.32;p≤0.005)。Fazekas 组之间的 BP-CBFV 相位和增益没有差异。在所有患者中,毛细血管相位和增益(CBFV-[O2Hb],CBFV-[HHb])与对照组相当。成功治疗的慢性 HBP 导致正常的脑毛细血管血液动力学,而阻力血管状态受到干扰(相位下降,增益增加)。