From the Department of Physiology, School of Medical Sciences, University of Auckland, Auckland, New Zealand.
Department of Anaesthesia and Perioperative Medicine, Auckland City Hospital, Auckland, New Zealand.
Anesth Analg. 2023 Aug 1;137(2):440-450. doi: 10.1213/ANE.0000000000006263. Epub 2022 Nov 9.
Intraoperative arterial hypotension (IOH) is a common side effect of general anesthesia (GA), associated with poor outcomes in ischemic stroke. While IOH is more prevalent with hypertension, it is unknown whether IOH may differ when GA is induced during ischemic stroke, versus other clinical settings. This is important given that many stroke patients receive GA for endovascular thrombectomy.
We evaluate the cardiovascular responses to volatile GA (isoflurane in 100% o2 ) before and during middle cerebral artery occlusion stroke in rats instrumented to record blood pressure (BP) and cerebral tissue oxygenation (p o2 ) in the projected penumbra, in clinically relevant cohorts of normotensive (Wistar rat, n = 10), treated hypertensive (spontaneously hypertensive [SH] + enalapril, n = 12), and untreated hypertensive (SH rat, n = 12).
During baseline induction of GA, IOH was similar in normotensive, treated hypertensive, and untreated hypertensive rats during the induction phase (first 10 minutes) (-24 ± 15 vs -28 ± 22 vs -48 ± 24 mm Hg; P > .05) and across the procedure (-24 ± 13 vs -30 ± 35 vs -39 ± 27 mm Hg; P > .05). Despite the BP reduction, cerebral p o2 increased by ~50% in all groups during the procedure. When inducing GA after 2 hours, all stroke groups showed a greater magnitude IOH compared to baseline GA induction, with larger falls in treated (-79 ± 24 mm Hg; P = .0202) and untreated(-105 ± 43 mm Hg; P < .001) hypertensive rats versus normotensives (-49 ± 21 mm Hg). This was accompanied by smaller increases in cerebral p o2 in normotensive rats (19% ± 32%; P = .0144 versus no-stroke); but a decrease in cerebral p o2 in treated (-11% ± 19%; P = .0048) and untreated (-12% ± 15%; P = .0003) hypertensive rats. Sham animals (normotensive and hypertensive) showed similar magnitude and pattern of IOH when induced with GA before and after sham procedure.
Our findings are the first demonstration that ischemic stroke per se increases the severity of IOH, particularly when combined with a prior history of hypertension; this combination appears to compromise penumbral perfusion.
术中动脉低血压（IOH）是全身麻醉（GA）的常见副作用，与缺血性中风的不良结局有关。虽然高血压时 IOH 更为常见，但在缺血性中风期间诱导 GA 与其他临床环境下是否会有不同，目前尚不清楚。鉴于许多中风患者接受 GA 进行血管内血栓切除术，这一点很重要。
我们评估了在大鼠模型中，在记录血压（BP）和预测半影区脑组织氧分压（p o2 ）的仪器上，在正常血压（Wistar 大鼠，n = 10）、治疗性高血压（自发性高血压[SH] + 依那普利，n = 12）和未治疗性高血压（SH 大鼠，n = 12）的临床相关亚组中，挥发性 GA（100% o2 中的异氟烷）诱导前后对大脑中动脉闭塞性中风的心血管反应。
在 GA 的基础诱导期间，正常血压、治疗性高血压和未治疗性高血压大鼠在诱导阶段（前 10 分钟）（-24 ± 15 对-28 ± 22 对-48 ± 24 mmHg；P >.05）和整个手术过程中（-24 ± 13 对-30 ± 35 对-39 ± 27 mmHg；P >.05），IOH 相似。尽管血压降低，但所有组在手术过程中大脑 p o2 增加了约 50%。当在 2 小时后诱导 GA 时，与基线 GA 诱导相比，所有中风组的 IOH 幅度更大，治疗性（-79 ± 24 mmHg；P =.0202）和未治疗性（-105 ± 43 mmHg；P <.001）高血压大鼠的下降幅度大于正常血压组（-49 ± 21 mmHg）。这伴随着正常血压大鼠大脑 p o2 增加幅度较小（19% ± 32%；P =.0144 与非中风组相比）；但治疗性（-11% ± 19%；P =.0048）和未治疗性（-12% ± 15%；P =.0003）高血压大鼠的大脑 p o2 下降。假手术动物（正常血压和高血压）在假手术前后用 GA 诱导时表现出相似的 IOH 幅度和模式。
我们的发现首次证明，缺血性中风本身会增加 IOH 的严重程度，特别是当与高血压病史相结合时；这种组合似乎会损害半影区灌注。
