医学
麻醉
异氟醚
冲程(发动机)
充氧
半影
血压
大脑中动脉
依那普利
缺血
内科学
心脏病学
血管紧张素转换酶
机械工程
工程类
作者
Tracy Zhang,Pratik Thakkar,Tonja W. Emans,Debra Fong,SumaMary Thampi,Igor Felippe,Carolyn J. Barrett,Robyn Billing,Douglas Campbell,Fiona D. McBryde
标识
DOI:10.1213/ane.0000000000006263
摘要
Background: 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. Methods: We evaluate the cardiovascular responses to volatile GA (isoflurane in 100% o 2 ) before and during middle cerebral artery occlusion stroke in rats instrumented to record blood pressure (BP) and cerebral tissue oxygenation (p o 2 ) 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). Results: 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 o 2 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 o 2 in normotensive rats (19% ± 32%; P = .0144 versus no-stroke); but a decrease in cerebral p o 2 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. Conclusions: 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.
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