Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

Juvela, Seppo

doi:10.3171/jns.2000.92.3.0390

Cited by 121 publications

(76 citation statements)

References 76 publications

(176 reference statements)

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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: 78%

“…29 -32. We also detected ET-1 in peripheral blood in the range of concentrations previously reported. 9 Systemic stress response could explain the release of ET-1 in the systemic circulation. Because levels in CSF were similar or even more elevated than in peripheral blood in many patients, ET-1 detected in CSF was unlikely to be derived only from the systemic circulation.…”

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

confidence: 99%

“…First, levels of ET-1 are increased in the cerebrospinal fluid (CSF) and plasma of SAH patients 3,4 in close correlation with development of vasospasm. [5][6][7][8][9] Second, delayed vasospasm can be experimentally evoked by the administration of ET-1. 10 -12 Third, antagonists of ET-1 attenuate vasospasm in experimental models of SAH.…”

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confidence: 99%

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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: 78%

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

confidence: 99%

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Endothelin-1 in Subarachnoid Hemorrhage

Faßbender

Hodapp

Rossol

et al. 2000

Stroke

140

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“…Endothelin (ET) levels increase after SAH (23,35), and the acute fall in cerebral blood flow after SAH in rats is attenuated by inhibitors of the synthesis of ET or ET receptor blockers (9). Enhanced turnover of fatty acids and increased formation of vasoconstrictor metabolites of arachidonic acid (AA) have also been observed after SAH (10,12).…”

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confidence: 99%

20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat

Kehl¹,

Cambj-Sapunar²,

Maier³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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man. 20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat. Am J Physiol Heart Circ Physiol 282: H1556-H1565, 2002. First published December 6, 2001 10.1152/ajpheart.00924.2001.-This study examined the effects of blocking the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) on the acute fall in cerebral blood flow after subarachnoid hemorrhage (SAH) in the rat. In vehicle-treated rats, regional cerebral blood flow (rCBF) measured with laser-Doppler flowmetry fell by 30% 10 min after the injection of 0.3 ml of arterial blood into the cisterna magna, and it remained at this level for 2 h. Pretreatment with inhibitors of the formation of 20-HETE, 17-octadecynoic acid (17-ODYA; 1.5 nmol intrathecally) and N-hydroxy-NЈ-(4-butyl-2-methylphenyl)formamidine (HET0016; 10 mg/kg iv), reduced the initial fall in rCBF by 40%, and rCBF fully recovered 1 h after induction of SAH. The concentration of 20-HETE in the cerebrospinal fluid rose from 12 Ϯ 2 to 199 Ϯ 17 ng/ml after SAH in vehicle-treated rats. 20-HETE levels averaged only 15 Ϯ 11 and 39 Ϯ 13 ng/ml in rats pretreated with 17-ODYA or HET0016, respectively. HET0016 selectively inhibited the formation of 20-HETE in rat renal microsomes with an IC50 of Ͻ15 nM and human recombinant CYP4A11, CYP4F2, and CYP4F3 enzymes with an IC50 of 42, 125, and 100 nM, respectively. These results indicate that 20-HETE contributes to the acute fall in rCBF after SAH in rats.

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“…De las tres isoformas conocidas, la ET-1 y la ET-3 han sido involucradas en la patofisiología del VC inducido por HSA. Aunque se han descrito algunas discrepancias, se reconoce que los pacientes que han sufrido una HSA tienen niveles altos de ET-1 y ET-3 en LCR y plasma 12,36,74 . Algunos autores han basado la polémica de la ET en el VC en que ésta también es producida por los astrocitos y en el hecho de que no siempre se ha encontrado una correlación clínica en pacientes con VC 25, 58 .…”

Section: Bloqueo De Espasmógenos: Antagonistas De Receptores Tipo a Dunclassified

Perspectivas en el tratamiento del vasospasmo cerebral inducido por hemorragia subaracnoidea

et al. 2007

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ResumenEl vasospasmo cerebral sigue siendo la causa más importante de invalidez y muerte posterior a la ruptura de aneurismas saculares intracerebrales. Las estrategias terapéuticas en el vasospasmo inducido por la hemorragia subaracnoidea pueden ser agrupadas en cuatro categorías a saber: 1) terapias de prevención; 2) terapias de reversión; 3) terapias para el aumento de la perfusión cerebral; y 4) terapias de neuroprotección y rescate. Estudios experimentales recientes han permitido la realización de estudios clínicos fase II que sugieren resultados positivos con medicamentos que incluyen estatinas (simvastatina y pravastatina) y antagonistas de receptores tipo A de la endotelina-1 (clasozentan). De igual manera, evidencias experimentales y clínicas han mostrado las ventajas del drenaje de líquido cefalorraquídeo, administración intratecal de donadores de óxido nítrico, y los efectos desinhibidores de la Ca2+ Protein Kinasa C (Fasudil) y catecolaminas sobre la vascularización cerebral. Este artículo resume el estado de investigación actual de posibles agentes y estrategias terapéuticas relevantes en el tratamiento del vasospasmo cerebral. .. I would caution that vasospasm is still around, it is still alive and living in every neurosurgical unit. Hence my plea that our scientists not falter or lose interest for a final understanding and solution"C.G. Drake,1990 9

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Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

Cited by 121 publications

References 76 publications

Endothelin-1 in Subarachnoid Hemorrhage

Endothelin-1 in Subarachnoid Hemorrhage

20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat

Perspectivas en el tratamiento del vasospasmo cerebral inducido por hemorragia subaracnoidea

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