Department of Neurosurgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
J Cereb Blood Flow Metab. 2021 Aug;41(8):1964-1977. doi: 10.1177/0271678X20983216. Epub 2021 Jan 18.
Alterations in the concentration of nitric oxide (NO) and L-arginine metabolites have been associated with the pathophysiology of different vascular diseases. Here, we describe striking changes in L-arginine metabolism after hemorrhagic stroke. Blood and cerebrospinal fluid (CSF) samples of patients with intracerebral hemorrhage (ICH) and/or intraventricular hemorrhage were collected over a ten-day period. Liquid chromatography-tandem mass spectrometry was used to quantify key substrates and products of L-arginine metabolizing enzymes as well as asymmetric (ADMA) and symmetric dimethylarginine (SDMA). Changes in the plasma were limited to early reductions in L-ornithine, L-lysine, and L-citrulline concentrations. Intrathecally, we observed signs of early NO synthase (NOS) upregulation followed by a decrease back to baseline accompanied by a rise in the level of its endogenous NOS-inhibitor ADMA. SDMA demonstrated increased levels throughout the observation period. For arginase, a pattern of persistently elevated activity was measured and arginine:glycine amidinotransferase (AGAT) appeared to be reduced in its activity at later time points. An early reduction in CSF L-arginine concentration was an independent risk factor for poor outcome. Together, these findings further elucidate pathophysiological mechanisms after ICH potentially involved in secondary brain injury and may reveal novel therapeutic targets.
一氧化氮(NO)和 L-精氨酸代谢物浓度的改变与不同血管疾病的病理生理学有关。在这里,我们描述了出血性中风后 L-精氨酸代谢的显著变化。在十天的时间内收集了脑出血(ICH)和/或脑室内出血患者的血液和脑脊液(CSF)样本。液相色谱-串联质谱法用于定量 L-精氨酸代谢酶的关键底物和产物以及不对称二甲基精氨酸(ADMA)和对称二甲基精氨酸(SDMA)。血浆中的变化仅限于早期 L-鸟氨酸、L-赖氨酸和 L-瓜氨酸浓度降低。鞘内,我们观察到早期一氧化氮合酶(NOS)上调的迹象,随后降至基线以下,同时其内源性 NOS 抑制剂 ADMA 水平升高。SDMA 在整个观察期间显示出升高的水平。对于精氨酸酶,测量到持续升高的活性模式,并且在稍后的时间点,精氨酸:甘氨酸酰胺转移酶(AGAT)的活性似乎降低。CSF 中 L-精氨酸浓度的早期降低是预后不良的独立危险因素。总之,这些发现进一步阐明了 ICH 后潜在涉及继发性脑损伤的病理生理机制,并可能揭示新的治疗靶点。