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Pharmacological evidence that potassium channels mediate hydrogen sulfide-induced inhibition of the vasopressor sympathetic outflow in pithed rats.药理学证据表明,钾通道介导了硫化氢诱导的麻醉大鼠血管加压素交感传出抑制。
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3
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Metab Brain Dis. 2022 Aug;37(6):1863-1874. doi: 10.1007/s11011-022-01033-1. Epub 2022 Jun 27.
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SAM, a cystathionine beta-synthase activator, promotes hydrogen sulfide to promote neural repair resulting from massive cerebral infarction induced by middle cerebral artery occlusion.SAM(半胱氨酸β-合酶激活剂)可促进内源性硫化氢产生,从而促进大脑中动脉闭塞所致大体积脑梗死的神经修复。
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The Slow-Releasing and Mitochondria-Targeted Hydrogen Sulfide (HS) Delivery Molecule AP39 Induces Brain Tolerance to Ischemia.慢释放和靶向线粒体的硫化氢(HS)递药分子 AP39 诱导脑对缺血的耐受。
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Endothelial glycocalyx in traumatic brain injury associated coagulopathy: potential mechanisms and impact.创伤性脑损伤相关凝血病中的内皮糖萼:潜在机制和影响。
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Inhalational Gases for Neuroprotection in Traumatic Brain Injury.吸入性气体在创伤性脑损伤中的神经保护作用。
J Neurotrauma. 2021 Oct 1;38(19):2634-2651. doi: 10.1089/neu.2021.0053. Epub 2021 Jun 8.

针对创伤后心血管损伤的硫化氢和一氧化氮靶向治疗。

Targeting hydrogen sulfide and nitric oxide to repair cardiovascular injury after trauma.

机构信息

Departamento de Farmacobiología, Cinvestav-Coapa, Mexico City, Mexico; Department of Pharmacology, University of Vermont, Burlington, VT, USA.

Departamento de Farmacobiología, Cinvestav-Coapa, Mexico City, Mexico.

出版信息

Nitric Oxide. 2022 Dec 1;129:82-101. doi: 10.1016/j.niox.2022.10.003. Epub 2022 Oct 22.

DOI:10.1016/j.niox.2022.10.003
PMID:36280191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10644383/
Abstract

The systemic cardiovascular effects of major trauma, especially neurotrauma, contribute to death and permanent disability in trauma patients and treatments are needed to improve outcomes. In some trauma patients, dysfunction of the autonomic nervous system produces a state of adrenergic overstimulation, causing either a sustained elevation in catecholamines (sympathetic storm) or oscillating bursts of paroxysmal sympathetic hyperactivity. Trauma can also activate innate immune responses that release cytokines and damage-associated molecular patterns into the circulation. This combination of altered autonomic nervous system function and widespread systemic inflammation produces secondary cardiovascular injury, including hypertension, damage to cardiac tissue, vascular endothelial dysfunction, coagulopathy and multiorgan failure. The gasotransmitters nitric oxide (NO) and hydrogen sulfide (HS) are small gaseous molecules with potent effects on vascular tone regulation. Exogenous NO (inhaled) has potential therapeutic benefit in cardio-cerebrovascular diseases, but limited data suggests potential efficacy in traumatic brain injury (TBI). HS is a modulator of NO signaling and autonomic nervous system function that has also been used as a drug for cardio-cerebrovascular diseases. The inhaled gases NO and HS are potential treatments to restore cardio-cerebrovascular function in the post-trauma period.

摘要

严重创伤,特别是神经创伤对心血管系统的全身性影响是创伤患者死亡和永久残疾的原因,需要治疗以改善预后。在一些创伤患者中,自主神经系统功能障碍会导致肾上腺素能过度刺激,导致儿茶酚胺持续升高(交感风暴)或阵发性交感神经活性的波动爆发。创伤还会激活先天免疫反应,将细胞因子和损伤相关分子模式释放到循环中。自主神经系统功能改变和广泛的全身炎症的这种组合会导致继发性心血管损伤,包括高血压、心肌损伤、血管内皮功能障碍、凝血功能障碍和多器官衰竭。气体递质一氧化氮(NO)和硫化氢(HS)是对血管张力调节具有强大作用的小气体分子。外源性 NO(吸入)在心脑血管疾病中有潜在的治疗益处,但有限的数据表明其在创伤性脑损伤(TBI)中有潜在的疗效。HS 是 NO 信号和自主神经系统功能的调节剂,也被用作心脑血管疾病的药物。吸入的气体 NO 和 HS 是恢复创伤后时期心脑血管功能的潜在治疗方法。