No Benefit of 3% Hypertonic Saline Following Experimental Intracerebral Hemorrhage.

IF 2.9 3区 医学 Q2 NEUROSCIENCES
Tiffany F C Kung, Anna C J Kalisvaart, Angely Claire C Suerte, Glen C Jickling, Frank K H van Landeghem, Frederick Colbourne
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引用次数: 0

Abstract

Intracerebral hemorrhage (ICH) is a stroke subtype with a high mortality rate (~ 40%). After ICH, the mass effect of the hematoma and edema contribute to raised intracranial pressure (ICP) and poor outcome. Endogenous compensatory mechanisms that blunt ICP elevations include redirection of venous blood and cerebrospinal fluid, along with brain tissue compliance (e.g., decreased cell volume, increased cell density); however, these limited reserves can be exhausted after severe stroke, resulting in decompensated ICP that requires careful clinical management. Management strategies can include administration of hypertonic saline (HTS), an osmotic agent that putatively attenuates edema, and thereby ICP elevations. Evidence regarding the efficacy of HTS treatment following ICH remains limited. In this study, adult male rats were given a collagenase-induced striatal ICH and a bolus of either 3% HTS or 0.9% saline vehicle at 2- and 14-hours post-stroke onset. Neurological deficits, edema, ipsilateral cell volume and density (in areas S1 and CA1), and contralateral CA1 ultrastructural morphology were assessed 24 h post-ICH. Animals had large bleeds (median 108.2 µL), extensive edema (median 83.9% brain water content in ipsilateral striatum), and evident behavioural deficits (median 5.4 neurological deficit scale score). However, HTS did not affect edema (p ≥ 0.4797), behaviour (p = 0.6479), cell volume (p ≥ 0.1079), or cell density (p ≥ 0.0983). Qualitative ultrastructural assessment of contralateral area CA1 suggested that HTS administration was associated with paradoxical cellular swelling in ICH animals. Overall, there was no benefit with administering 3% HTS after ICH.

实验性脑出血后使用 3% 高渗盐水无益。
脑出血(ICH)是一种死亡率很高(约 40%)的中风亚型。ICH 后,血肿和水肿的肿块效应导致颅内压(ICP)升高,预后不良。钝化 ICP 升高的内源性代偿机制包括静脉血和脑脊液的重新定向,以及脑组织的顺应性(如细胞体积减少、细胞密度增加);然而,这些有限的储备在严重卒中后可能会耗尽,导致 ICP 失代偿,需要谨慎的临床管理。处理策略包括使用高渗盐水(HTS),这是一种渗透剂,可减轻水肿,从而缓解 ICP 升高。有关 ICH 后 HTS 治疗效果的证据仍然有限。在这项研究中,成年雄性大鼠接受了胶原酶诱导的纹状体 ICH,并在中风发作后 2 小时和 14 小时分别注射了 3% HTS 或 0.9% 生理盐水。对中风后 24 小时的神经功能缺损、水肿、同侧细胞体积和密度(S1 和 CA1 区域)以及对侧 CA1 超微结构形态进行了评估。动物有大量出血(中位数为 108.2 µL)、广泛水肿(同侧纹状体脑水含量中位数为 83.9%)和明显的行为障碍(神经功能缺损量表评分中位数为 5.4 分)。然而,HTS 不会影响水肿(p ≥ 0.4797)、行为(p = 0.6479)、细胞体积(p ≥ 0.1079)或细胞密度(p ≥ 0.0983)。对侧 CA1 区的定性超微结构评估表明,HTS 给药与 ICH 动物的矛盾细胞肿胀有关。总体而言,在 ICH 后施用 3% HTS 没有任何益处。
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来源期刊
Neurotoxicity Research
Neurotoxicity Research 医学-神经科学
CiteScore
7.70
自引率
5.40%
发文量
164
审稿时长
6-12 weeks
期刊介绍: Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.
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