Cerebrospinal fluid endothelin-1 and endothelin-3 levels in normal and neurosurgical patients: A clinical study and literature review

Kraus, Gary E.; Bucholz, Richard D.; Yoon, Kong-Woo; Knuepfer, Mark M.; Smith, Kenneth R.

doi:10.1016/0090-3019(91)90197-h

Cited by 94 publications

(30 citation statements)

References 49 publications

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“…Also consistent with our observation was the reported enhanced vasoconstriction to ET-1 in cerebral arteries from rats with subarachnoid hemorrhage (36). Increased synthesis of vasoconstrictors LTC,, ET-1, thromboxane B,, and PGF,, has been reported in newborn and adult animal models, as well as in human patients with subarachnoid hemorrhage (6,8,14,23,37). Furthermore, in adult animal models of subarachnoid hemorrhage and in clinical cases, reduced dilator prostanoid synthesis and increased constrictor prostanoid synthesis have been observed (4,6,8).…”

Section: Sahsupporting

confidence: 90%

“…Increased secretion of spasmogenic agents such as PGF,,, LTC,, and ET-1 have been reported after hemorrhage (8,(18)(19)(20). Studies in adult humans showed elevated levels of vasoconstrictor agents: thromboxanes, leukotrienes, PGF,,, ET-1, and oxyhemoglobin in the cerebrospinal fluid after subarachnoid hemorrhage (6)(7)(8)(21)(22)(23)(24)(25). Hence, eicosanoid and endothelin production systems could contribute to inappropriate cerebral vasoconstriction after subarachnoid hemorrhage.…”

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confidence: 99%

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Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs

1994

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The effects of perivascular blood on pial arteriolar vasoreactivity to selected vasodilators and vasoconstrictors were examined in vivo in a newborn pig model. a-Chloraloseanesthetized newborn pigs were fitted with closed cranial windows 4 d after cortical subarachnoid injections of autologous blood. The responsiveness of pial arterioles to topical application of dilator agents [iloprost, prostaglandin E, (PGE,), histamine, and sodium nitroprusside (SNP)] and vasoconstrictor agents [leukotriene C4 and endothelin-1 (ET-1) in artificial cerebrospinal fluid was studied in control and blood-injected piglets. Pial arterioles dilated dose dependently in response to topical application of iloprost, PGE,, histamine, and SNP in the control group, with increases in diameter of 54,44,67, and 50% at lop8 M, lop5 M, lop5 M, and M, respectively. These dilations in response to iloprost, PG&, and histamine in the blood-injected piglets were significantly attenuated to 23, 18, and 34%, respectively, whereas the dilation in response to SNP was not changed (64%). Constrictions in response to lop8 M leukotriene C4 and ET-1 were 16 and 26% and were potentiated by hematoma to 36 and 43%, respectively. The lowest dose of ET-1 (10-l2 M) significantly dilated pial arterioles in the control but not in the blood-treated group. We conclude that prolonged exposure of pial arterioles to perivascular blood attenuates cerebrovascular dilation in response to selected vasoactive agents (iloprost, PGE;, and histamine) but not to SNP, suggesting that blood-induced attenuation of vasodilation and the generalized vasoconstriction may involve inhibiting the prostanoid/cAMP signaling pathway. Potentiation of vasoconstriction induced by ET-1 and leukotriene C, in the hematoma group could be due to loss of this dilator influence. (Pediatr Res 36: [589][590][591][592][593][594] 1994) Abbreviations aCSF, artificial cerebrospinal fluid ET-1, endothelin-1 LTC,, leukotriene C, PGF,, prostaglandin F,, PGE,, prostaglandin E, SNP, sodium nitroprusside Intraventricular and periventricular cerebral hemorrhages occur frequently in preterm babies, whereas subarachnoid hemorrhages occur in both term and preterm infants (1-3). In adults and children, subarachnoid hemorrhage can also result from trauma, asphyxia, brain injury, or rupture of an intracranial aneurysm (4-6). In adults, one of the major complications of cerebral hemorrhage is a delayed cerebral ischemia due to abnormal vasoconstriction of large cerebral arteries that usually presents itself 4-7 d after the hemorrhage. Alterations of cerebral circulation and metabolism can develop secondary to cerebral vasoconstriction, resulting in death or permanent cerebral dysfunction (4-8). Despite much research into the etiology of hemorrhage-induced vasoconstriction (4-8), our understanding of the mechanism by which cerebral arterial vasoconstriction occurs after cerebral hemorrhages is still limited. Much less information is available on the effects of hematoma on cerebral circulation in neonates.Vasodilator pr...

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Section: Sahsupporting

confidence: 90%

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confidence: 99%

Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs

1994

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“…Endothelin signaling is activated at the site of vascular injury, 12,25 causing cell proliferation; indeed, after SAH, EDNRA and endothelin-1 protein levels are both increased in CSF. [26][27][28] Alternatively, downregulation of EDNRA signaling could lead to defective vascular repair, allowing aneurysms to develop after injury, a hypothesis supported by functional analysis of EDNRA variants showing lower transcriptional activity for the rs6841581 risk allele (G). 13 SNPs with unknown function or not examined in more than 2 studies.…”

Section: -252)mentioning

confidence: 99%

Genetic risk factors for intracranial aneurysms

et al. 2013

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A meta-analysis in more than 116,000 individuals ABSTRACT Objective: There is an urgent need to identify risk factors for sporadic intracranial aneurysm (IA) development and rupture. A genetic component has long been recognized, but firm conclusions have been elusive given the generally small sample sizes and lack of replication. Genome-wide association studies have overcome some limitations, but the number of robust genetic risk factors for IA remains uncertain. Methods:We conducted a comprehensive systematic review and meta-analysis of all genetic association studies (including genome-wide association studies) of sporadic IA, conducted according to Strengthening the Reporting of Genetic Association Studies and Human Genome Epidemiology Network guidelines. We tested the robustness of associations using random-effects and sensitivity analyses.Results: Sixty-one studies including 32,887 IA cases and 83,683 controls were included. We identified 19 single nucleotide polymorphisms associated with IA. The strongest associations, robust to sensitivity analyses for statistical heterogeneity and ethnicity, were found for the following single nucleotide polymorphisms: on chromosome 9 within the cyclin-dependent kinase inhibitor 2B antisense inhibitor gene (rs10757278: odds ratio [OR] 1.29; 95% confidence interval [CI] 1.21-1.38; and rs1333040: OR 1.24; 95% CI 1.20-1.29), on chromosome 8 near the SOX17 transcription regulator gene (rs9298506: OR 1.21; 95% CI 1.15-1.27; and rs10958409: OR 1.19; 95% CI 1.13-1.26), and on chromosome 4 near the endothelin receptor A gene (rs6841581: OR 1.22; 95% CI 1.14-1.31). Conclusions:Our comprehensive meta-analysis confirms a substantial genetic contribution to sporadic IA, implicating multiple pathophysiologic pathways, mainly relating to vascular endothelial maintenance. However, the limited data for IA compared with other complex diseases necessitates large-scale replication studies in a full spectrum of populations, with investigation of how genetic variants relate to phenotype (e.g., IA size, location, and rupture status). Neurology â 2013;80:2154-2165 GLOSSARY ACE 5 angiotensin-converting enzyme; ANRIL 5 antisense noncoding RNA in the INK4 locus; CI 5 confidence interval; CGAS 5 candidate gene association study; EDNRA 5 endothelin receptor type A; GWAS 5 genome-wide association studies; IA 5 intracranial aneurysm; IL 5 interleukin; LD 5 linkage disequilibrium; MMP 5 matrix metalloproteinase; OR 5 odds ratio; SAH 5 subarachnoid hemorrhage; SNP 5 single nucleotide polymorphism.Intracranial aneurysms (IAs) are present in 2%-5% of the general population; approximately 0.7%-1.9% of cases rupture, causing subarachnoid hemorrhage (SAH).1 The annual incidence of SAH is 8-9 in 100,000, yet because of the high risk of death or severe disability 2 and younger age at onset compared with other stroke types (40-65 years), 3 SAH has a disproportionately large socioeconomic impact.SAH has been associated with common modifiable risk factors, including hypertension, smoking, and alcohol intake. [4][...

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“…Because of its potent and long-lasting constrictor action on cerebral arteries (202,203), much of the interest surrounding endothelin-1 in the central nervous system evolves around its putative role as a causative or modulatory factor of cerebral vasospasm. Elevated levels of endothelin-1 in the plasma and/or cerebrospinal fluid have been documented in patients suffering from acute cerebral events associated with cerebral artery spasm (204)(205)(206)(207). The inhibition of mRNA transcription by actinomycin D greatly ameliorated the development of chronic cerebral vasospasm in dogs (208), implying that endothelin-1 or other peptides may be involved in the pathogenesis of vasospasm.…”

Section: V-4 Brain Injury and Cerebral Vasospasmmentioning

confidence: 99%

Molecular Pharmacology and Pathophysiological Significance of Endothelin

Goto

Hama

Kasuya

1996

Japanese Journal of Pharmacology

159

108

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ABSTRACT-Since the discovery of the most potent vasoconstrictor peptide, endothelin, in 1988, explosive investigations have rapidly clarified much of the basic pharmacological, biochemical and molecular biological features of endothelin, including the presence and structure of isopeptides and their genes (endothelin-1, -2 and -3), regulation of gene expression, intracellular processing, specific endothelia converting enzyme (ECE), receptor subtypes (ETA and ETB), intracellular signal transduction following receptor activation, etc. ECE was recently cloned, and its structure was shown to be a single transmembrane protein with a short intracellular N-terminal and a long extracellular C-terminal that contains the catalytic domain and numerous N-glycosylation sites. In addition to acute contractile or secretory actions, endothelin has been shown to exert long-term proliferative actions on many cell types. In this case, intracellular signal transduction appears to converge to activation of mitogen-activated protein kinase. As a recent dramatic advance, a number of non-peptide and orally active receptor antagonists have been developed. They, as well as current peptide antagonists, markedly accelerated the pace of investigations into the true pathophysiological roles of endogenous endothelin-1 in mature animals; e.g., hypertension, pulmonary hypertension, acute renal failure, cerebral vasospasm, vascular thickening, cardiac hypertrophy, chronic heart failure, etc. Thus, the interference with the endothelin pathway by either ECE-inhibition or receptor blockade may

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Cerebrospinal fluid endothelin-1 and endothelin-3 levels in normal and neurosurgical patients: A clinical study and literature review

Cited by 94 publications

References 49 publications

Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs

Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs

Genetic risk factors for intracranial aneurysms

Molecular Pharmacology and Pathophysiological Significance of Endothelin

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