Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Kessler, Iruena Moraes; Pacheco, Yolanda Galindo; Lozzi, Silene P.; Araújo, António; Onishi, Franz Jooji; Mello, Paulo Andrade de

doi:10.1016/j.surneu.2005.04.014

Cited by 43 publications

(36 citation statements)

References 20 publications

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“…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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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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“…Suzuki and associates reported increased levels of ET-1 in the CSF of aSAH patients (Suzuki, Sato, Suzuki, Takekoshi, et al, 1990). Recent studies showed that increased CSF ET-1 levels are associated with the development of CV after aSAH (Kessler, Pacheco, Lozzi, de Araujo, Onishi, de Mello, et al, 2005), thus supporting the role of ET-1 in the pathogenesis of CV.…”

Section: Discussionmentioning

confidence: 82%

Endothelin-1 and Endothelin Receptor Gene Variants and Their Association With Negative Outcomes Following Aneurysmal Subarachnoid Hemorrhage

Gallek

Alexander

Crago

et al. 2012

Biological Research For Nursing

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Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease that affects approximately 30,000 people a year in the United States. Delayed cerebral ischemia (DCI) and cerebral vasospasm (CV) are common complications after aSAH. In addition, aSAH patients have a high risk of poor long-term outcomes. Endothelin-1 (ET-1), a potent vasoconstrictor, or its two types of receptors, ET receptor A (ETA ) and ET receptor B (ETB), may play a role in the pathogenesis of DCI and CV. Genetic variations within the ET-1, ETA, or ETB genes may also account for variance observed in the outcomes of aSAH patients. The purpose of this study was to describe the distribution of the Lys198Asn polymorphism, a known functional SNP in the ET-1 gene, and tagging SNPs of the ET-1, ETA, and ETB genes in individuals recovering from aSAH. This study also investigated the relationships among the ET polymorphisms, DCI, and global functional outcomes measured at 3 and 6 months after aSAH. Participants included individuals aged 18–75 years with a diagnosis of aSAH. There was a trend found between the variant allele of an ET-1 SNP (rs6912834) and angiographic vasospasm. There were also associations found between two ETB SNPs (rs9574124 and rs3027111) and poor outcomes as measured by the Glasgow Outcome scale at 3 months. These findings support the role of ET-1 and ETB in recovery following aSAH.

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“…Acting in concert with other vasoactive factors, ETs may contribute substantially to the disturbed equilibrium between constriction and relaxation that typifies vascular responses following SAH. Endothelin concentrations in plasma or CSF correlate with delayed cerebral ischemia and vasospasm after SAH, with the highest levels of ET predicting cerebral ischemia and symptomatic vasospasm [51, 52]. The potential involvement of ET in cerebral vasospasm following SAH has triggered considerable interest in designing therapeutic strategies to inhibit biological effects of ET.…”

Section: Reviewmentioning

confidence: 99%

Unfractionated Heparin: Multitargeted Therapy for Delayed Neurological Deficits Induced by Subarachnoid Hemorrhage

et al. 2010

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Aneurysmal subarachnoid hemorrhage (SAH) is associated with numerous “delayed neurological deficits” (DNDs) that have been attributed to multiple pathophysiological mechanisms, including ischemia, microthrombosis, free radical damage, inflammation, and vascular remodeling. To date, effective prophylactic therapy for SAH-induced DNDs has been elusive, due perhaps to the multiplicity of mechanisms involved that render typical, single-agent therapy seemingly futile. We hypothesized that heparin, which has multiple underappreciated salutary effects, might be useful as a multitargeted prophylactic agent against SAH-induced DNDs. We performed a comprehensive review of the literature to evaluate the potential utility of heparin in targeting the multiple pathophysiological mechanisms that have been identified as contributing to SAH-induced DNDs. Our literature review revealed that unfractionated heparin can potentially antagonize essentially all of the pathophysiological mechanisms known to be activated following SAH. Heparin binds >100 proteins, including plasma proteins, proteins released from platelets, cytokines, and chemokines. Also, heparin complexes with oxyhemoglobin, blocks the activity of free radicals including reactive oxygen species, antagonizes endothelin-mediated vasoconstriction, smooth muscle depolarization, and inflammatory, growth and fibrogenic responses. Our review suggests that the use of prophylactic heparin following SAH may warrant formal study.

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Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Cited by 43 publications

References 20 publications

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

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

Endothelin-1 and Endothelin Receptor Gene Variants and Their Association With Negative Outcomes Following Aneurysmal Subarachnoid Hemorrhage

Unfractionated Heparin: Multitargeted Therapy for Delayed Neurological Deficits Induced by Subarachnoid Hemorrhage

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