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Therapeutic Relevance of Elevated Blood Pressure After Ischemic Stroke in the Hypertensive Rats
Hypertension ( IF 6.9 ) Pub Date : 2020-03-01 , DOI: 10.1161/hypertensionaha.119.14219
Pratik C Thakkar 1 , Ailsa L McGregor 2 , P Alan Barber 3 , Julian F R Paton 1 , Carolyn J Barrett 1 , Fiona D McBryde 1
Affiliation  

Supplemental Digital Content is available in the text. Over 80% of patients exhibit an acute increase in blood pressure (BP) following stroke. Current clinical guidelines make no distinction in BP management between patients with or without prior hypertension. Spontaneously hypertensive (SH) rats were preinstrumented with telemeters to record BP, intracranial pressure, and brain tissue oxygen in the predicted ischemic penumbra for 3 days before and 10 days after transient middle cerebral artery occlusion (n=8 per group) or sham (n=5). Before stroke, BP was either left untreated or chronically treated to a normotensive level (enalapril 10 mg/kg per day). Poststroke elevations in BP were either left uncontrolled, controlled (to the prestroke baseline level), or overcontrolled (to a normotensive level) via subcutaneous infusion of labetalol. Baseline values of intracranial pressure and brain tissue oxygen were similar between all groups, whereas BP was lower in treated SH rats (144±3 versus 115±5 mm Hg; P<0.001). Following middle cerebral artery occlusion, a similar rise in BP was observed in untreated (+16±2 mm Hg; P=0.005) and treated SH rats (+13±5 mm Hg; P=0.021). Intervening to prevent BP from increasing after stroke did not worsen outcome. However, reducing BP below prestroke baseline levels was associated with higher intracranial pressure (days 1–3; P<0.001), reduced cerebral perfusion pressure (days 2–4; P<0.001), higher mortality, slower functional recovery and larger infarct volumes. Although treating to maintain BP at the prestroke baseline level was not detrimental, our results suggest that when setting BP targets after stroke, consideration must be given to the potential negative impact of inadvertent excessive BP lowering in subjects with undiagnosed or poorly controlled hypertension.

中文翻译:

高血压大鼠缺血性脑卒中后血压升高的治疗意义

补充数字内容在文本中可用。超过 80% 的患者在中风后表现出血压 (BP) 急剧升高。目前的临床指南对既往有或没有高血压的患者的血压管理没有区别。自发性高血压 (SH) 大鼠预先用遥测仪记录血压、颅内压和脑组织氧在预测的缺血半暗带中的 3 天和 10 天的短暂大脑中动脉闭塞(每组 n = 8)或假手术(n =5)。在中风之前,BP 要么未经治疗,要么长期治疗至正常血压水平(依那普利 10 毫克/公斤/天)。中风后血压升高要么不受控制,要么通过皮下输注拉贝洛尔得到控制(达到中风前的基线水平)或过度控制(达到正常血压水平)。所有组的颅内压和脑组织氧的基线值相似,而治疗的 SH 大鼠的血压较低(144±3 对 115±5 mm Hg;P<0.001)。大脑中动脉闭塞后,在未治疗(+16±2 mm Hg;P=0.005)和治疗的 SH 大鼠(+13±5 mm Hg;P=0.021)中观察到类似的血压升高。干预以防止卒中后血压升高并未使结果恶化。然而,将血压降低至卒中前基线水平以下与颅内压升高(第 1-3 天;P<0.001)、脑灌注压降低(第 2-4 天;P<0.001)、更高的死亡率、更慢的功能恢复和更大的梗死体积相关. 尽管将血压维持在卒中前基线水平的治疗无害,但我们的结果表明,在卒中后设定血压目标时,
更新日期:2020-03-01
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