医学
脑水肿
冲程(发动机)
水肿
麻醉
NK1受体拮抗剂
颅内压
敌手
P物质
缺血
脑血流
内科学
受体
神经肽
机械工程
工程类
作者
Annabel Sorby‐Adams,Oana C. Marian,Isabella M. Bilecki,Levi E. Elms,Nawaf Yassi,Rebecca J. Hood,Janet K. Coller,Shannon M. Stuckey,W. Taylor Kimberly,Tracy D. Farr,Anna V. Leonard,Emma Thornton,Robert Vink,Renée J. Turner
标识
DOI:10.1177/0271678x241241907
摘要
Following ischemic stroke, substance P (SP)-mediated neurogenic inflammation is associated with profound blood-brain barrier (BBB) dysfunction, cerebral edema, and elevated intracranial pressure (ICP). SP elicits its effects by binding the neurokinin 1 tachykinin receptor (NK1-R), with administration of an NK1-R antagonist shown to ameliorate BBB dysfunction and cerebral edema in rodent and permanent ovine stroke models. Given the importance of reperfusion in clinical stroke, this study examined the efficacy of NK1-R antagonist treatment in reducing cerebral edema and ICP in an ovine model of transient middle cerebral artery occlusion (tMCAo). Anesthetized sheep ( n = 24) were subject to 2-hours tMCAo and randomized ( n = 6/group) to receive early NK1-R treatment (days 1–3 post-stroke), delayed NK1-R treatment (day 5 post-stroke), or saline vehicle. At 6-days post-stroke animals were re-anaesthetized and ICP measured, followed by MRI to evaluate infarction, edema and BBB dysfunction. Following both early and delayed NK1-R antagonist administration, ICP was significantly reduced on day 6 compared to vehicle animals (p < 0.05), accompanied by a reduction in cerebral edema, midline shift and BBB dysfunction (p < 0.05). This study demonstrates that NK1-R antagonist treatment is an effective novel therapy for cerebral edema and elevated ICP following stroke in an ovine model, warranting future clinical evaluation.
科研通智能强力驱动
Strongly Powered by AbleSci AI