Österlind Jonas, Birnefeld Johan, Eklund Anders, Hultin Magnus, Wåhlin Anders, Holmlund Petter, Zarrinkoob Laleh
Department of Diagnostics and Intervention, Anesthesiology and Intensive Care, Umeå University, Umeå, Sweden.
Department of Clinical Sciences, Neurosciences, Umeå University, Umeå, Sweden.
Anesthesiology. 2025 Oct 1;143(4):917-928. doi: 10.1097/ALN.0000000000005651. Epub 2025 Jul 11.
Induced hypertension is used clinically to increase cerebral blood flow (CBF) in conditions such as vasospasm after subarachnoid hemorrhage. However, increased blood pressure also raises pulsatile force. Cerebrovascular compliance plays a key role in buffering flow dynamics and protecting the microcirculation, but whether it adapts to elevated pressure remains unclear. This study assessed the response of compliant cerebral arteries to induced hypertension in healthy adults using phase-contrast magnetic resonance imaging (PCMRI) and two compliance models: a two-element Windkessel (compliance estimated using the Windkessel model, C WK ) and a simplified model (compliance calculated as the ratio of pulsatile volume to pressure, C VP ), representing the extremes of pulsatility transmission at the capillary level.
Eighteen healthy adults (median age, 34 yr; nine women) underwent PCMRI at baseline and after increasing mean arterial pressure by 20% using norepinephrine infusion. PCMRI quantified CBF and cardiac output, while cerebrovascular resistance and systemic vascular resistance were derived. Flow waveforms were combined with blood pressure to assess C WK and C VP in CBF, ascending/descending aorta, and external carotid arteries, while corresponding regions of interest were used to calculate cross-sectional flow areas. Data are reported as median (interquartile range).
Norepinephrine increased cerebrovascular compliance significantly: C WK by 110% (56 to 163%; P = 0.001) and C VP by 11% (-2 to 26%; P = 0.018). C WK increased in the external carotid artery by 12% (1 to 32%; P = 0.037) but did not change in the ascending or descending aorta. C VP decreased in the descending aorta by 5% (-11 to 2%; P = 0.028), with no changes in the ascending aorta or external carotid artery. Cross-sectional area of cerebral arteries contributing to CBF decreased by 5% (-17 to -3%; P = 0.033), while the ascending and descending aorta areas increased by 7% (4 to 11%; P = 0.012) and 8% (6 to 11%; P < 0.001), respectively.
Cerebral arteries enhanced their compliance during norepinephrine-induced hypertension, unlike systemic arteries, regardless of the assumed degree of pulsatility transmission.
在蛛网膜下腔出血后血管痉挛等情况下,临床使用诱导性高血压来增加脑血流量(CBF)。然而,血压升高也会增加搏动力量。脑血管顺应性在缓冲血流动力学和保护微循环方面起着关键作用,但它是否能适应血压升高仍不清楚。本研究使用相位对比磁共振成像(PCMRI)和两种顺应性模型,评估健康成年人中顺应性脑动脉对诱导性高血压的反应:双元件风箱模型(使用风箱模型估计的顺应性,C_WK)和简化模型(顺应性计算为搏动容积与压力之比,C_VP),分别代表毛细血管水平搏动性传递的两个极端情况。
18名健康成年人(中位年龄34岁;9名女性)在基线时以及使用去甲肾上腺素输注将平均动脉压升高20%后接受PCMRI检查。PCMRI定量测量CBF和心输出量,同时推导脑血管阻力和全身血管阻力。将血流波形与血压相结合,评估CBF、升主动脉/降主动脉和颈外动脉中的C_WK和C_VP,同时使用相应的感兴趣区域计算横截面积。数据报告为中位数(四分位间距)。
去甲肾上腺素显著增加了脑血管顺应性:C_WK增加了110%(56%至163%;P = 0.001),C_VP增加了11%(-2%至26%;P = 0.018)。颈外动脉的C_WK增加了12%(1%至32%;P = 0.037),但升主动脉或降主动脉中的C_WK没有变化。降主动脉中的C_VP下降了5%(-11%至2%;P = 0.028),升主动脉或颈外动脉中的C_VP没有变化。对CBF有贡献的脑动脉横截面积减少了5%(-17%至-3%;P = 0.033),而升主动脉和降主动脉的面积分别增加了7%(4%至11%;P = 0.012)和8%(6%至11%;P < 0.001)。
在去甲肾上腺素诱导的高血压期间,脑动脉增强了其顺应性,与全身动脉不同,无论假定的搏动性传递程度如何。