Endothelin-1 concentration increases in the cerebrospinal fluid in cerebral vasospasm caused by subarachnoid hemorrhage

Suzuki, Kensuke; Meguro, Kotoo; Sakurai, Takeshi; Saitoh, Yoshifumi; Takeuchi, Sawako; Nose, Tadao

doi:10.1016/s0090-3019(99)00179-2

Cited by 40 publications

(29 citation statements)

References 19 publications

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“…Our observation that subjects with evidence of severe vasospasms (higher CBFV) exhibit higher ET-1 concentrations in CSF is in accordance with some [5][6][7][8][9]35 but not all 9 earlier studies that reported possible associations between ET-1 levels and cerebrovascular complications. It must be noted that ET-1 may also act in a paracrine fashion 36 ; therefore, a strong correlation between ET-1 concentration and vasospasm is not mandatory to establish the pathogenetic importance of ET-1 in SAH.…”

Section: Faßbender Et Al Et-1 In Subarachnoid Hemorrhage 2973supporting

confidence: 91%

Endothelin-1 in Subarachnoid Hemorrhage

Faßbender

Hodapp

Rossol

et al. 2000

Stroke

140

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Background and Purpose-The most potent vasoconstrictor known, endothelin-1, is currently considered to mediate cerebral vasospasm in subarachnoid hemorrhage (SAH), which can cause delayed cerebral ischemia. In our study, we performed clinical and in vitro experiments to investigate the origin and the mechanisms of the secretion of endothelin-1 in SAH. Methods-Endothelin-1 and markers of inflammatory host response (interleukin [IL]-1␤, IL-6, and tumor necrosis factor-␣) were comparatively quantified in the cerebrospinal fluid (CSF) of SAH patients and control subjects, and concentrations were related to clinical characteristics. Furthermore, mononuclear leukocytes isolated from the CSF of SAH patients and control subjects were analyzed regarding their mRNA expression of endothelin-1 and inflammatory cytokines. Finally, complementary in vitro experiments were performed to investigate whether coincubation of blood and CSF can trigger leukocytic mRNA expression and release of these factors. Results-Activated mononuclear leukocytes in the CSF of SAH patients synthesize and release endothelin-1 in parallel with known acute-phase reactants (IL-1␤, IL-6, and tumor necrosis factor-␣). Complementary in vitro experiments not only further confirmed this leukocytic origin of endothelin-1 but also showed that aging and subsequent hemolysis of blood is sufficient to induce such endothelin-1 production. Conclusions-The demonstration that endothelin-1 is produced by activated CSF mononuclear leukocytes suggests that subarachnoid inflammation may represent a therapeutic target to prevent vasospasm and delayed cerebral ischemia after SAH. (Stroke. 2000;31:2971-2975.)

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Section: Faßbender Et Al Et-1 In Subarachnoid Hemorrhage 2973supporting

confidence: 91%

Endothelin-1 in Subarachnoid Hemorrhage

Faßbender

Hodapp

Rossol

et al. 2000

Stroke

140

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show abstract

“…ET-1 concentrations in the CSF of patients after SAH were significantly elevated compared with control groups, consisting mainly of healthy volunteers and patients with another neurologic nonhemorrhagic disease, such as hydrocephalus or degenerative spinal disease. [2][3][4][5][6][7][8] In patients who did not develop CV, ET-1 concentrations decreased gradually with time, 6,8 whereas CV patients exhibited a significant increase between days 4 and 7 posthemorrhage and postsurgery. 3,8,9 This increase coincided with the occurrence of symptomatic CV.…”

Section: Endothelin-1mentioning

confidence: 99%

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

Lad¹,

Hegen²,

Gupta³

et al. 2012

Journal of Stroke and Cerebrovascular Diseases

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“…Several studies showed a secondary rise in ET-1 coinciding with the development of cerebral vasospasm, whereas there was no rise in ET-1 in those without vasospasm [14]. Endothelins are also presumed to have a significant effect on secondary brain injury after TBI, with many putative roles ascribed to the ET A and ET B receptors in animal models [15][16][17].…”

Section: Introductionmentioning

confidence: 99%