Endothelin-1 levels in plasma and cerebrospinal fluidfollowing subarachnoid haemorrhage

Kobayashi, Hidenori; Ide, Hisashi; Ishii, Hisamasa; Kabuto, Masanori; Handa, Yuji; Kubota, Toshihiko

doi:10.1016/s0967-5868(95)80011-5

Cited by 11 publications

(12 citation statements)

References 37 publications

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“…Three hours after SAH: Cerebral NO level is increasing towards recovery [59], platelet aggregates are still present in the cerebral vessels [62], oxidative stress persists [77, 78], and inflammatory cytokines are expressed. Twenty-four hours after SAH: Cerebral NO level increases above basal value [60, 61], platelet aggregation in parenchymal vessels continues [62], plasma ET-1 level remains increased [73], oxidative stress persists [145], expression of inflammatory cytokine persists [144], and their markers appear in serum and CSF [88]. Seventy-four hours after SAH: CSF level of NO [61] and of ET-1 is increased [73], oxidative stress persists [145], CSF inflammatory cytokine level remains increased [88], and blood platelet count remains decreased indicating activation, sequestration/aggregation in the brain [146].…”

Section: Early Brain Injury By Sahmentioning

confidence: 99%

“…Twenty-four hours after SAH: Cerebral NO level increases above basal value [60, 61], platelet aggregation in parenchymal vessels continues [62], plasma ET-1 level remains increased [73], oxidative stress persists [145], expression of inflammatory cytokine persists [144], and their markers appear in serum and CSF [88]. Seventy-four hours after SAH: CSF level of NO [61] and of ET-1 is increased [73], oxidative stress persists [145], CSF inflammatory cytokine level remains increased [88], and blood platelet count remains decreased indicating activation, sequestration/aggregation in the brain [146]. Insert : Antioxidant system activity is decreased and lipid peroxidation products accumulate within 72 h after SAH and correlate well with poor clinical conditions and outcome [79, 145]…”

Section: Early Brain Injury By Sahmentioning

confidence: 99%

“…ET-1 is implicated in early brain injury and in the pathogenesis of delayed vasospasm and delayed ischemic deficits after SAH [70–72]. A number of observations support this concept: (1) ET-1 level increases in serum and plasma within minutes after SAH and expression of its receptors increases 24 to 48 h later [73–75]; (2) ET-1 has the capacity to produce long-lasting constriction [73]; (3) ET-1 level is increased at the time that cerebral NO is reduced (see above) and thus has a perfect unopposed opportunity to elicit a sustained contraction in cerebral vessels after SAH; and (4) ET-1 creates the degenerative morphological changes in the vascular wall similar to those that occur after SAH [76]. Therefore, ET-1 provides yet another mechanism that activates minutes after SAH and has early, delayed, and prolonged consequences.…”

Section: Early Brain Injury By Sahmentioning

confidence: 99%

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Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury

2010

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Delayed vasospasm that develops 3–7 days after aneurysmal subarachnoid hemorrhage (SAH) has traditionally been considered the most important determinant of delayed ischemic injury and poor outcome. Consequently, most therapies against delayed ischemic injury are directed towards reducing the incidence of vasospasm. The clinical trials based on this strategy, however, have so far claimed limited success; the incidence of vasospasm is reduced without reduction in delayed ischemic injury or improvement in the long-term outcome. This fact has shifted research interest to the early brain injury (first 72 h) evoked by SAH. In recent years, several pathological mechanisms that activate within minutes after the initial bleed and lead to early brain injury are identified. In addition, it is found that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome. Therefore, a therapy or therapies focused on these early mechanisms may not only prevent the early brain injury but may also help reduce the intensity of later developing neurological complications. This manuscript reviews the pathological mechanisms of early brain injury after SAH and summarizes the status of current therapies.

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Section: Early Brain Injury By Sahmentioning

confidence: 99%

Section: Early Brain Injury By Sahmentioning

confidence: 99%

Section: Early Brain Injury By Sahmentioning

confidence: 99%

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Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury

2010

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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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“…En effet, les concentrations d'ET-1 augmentent dans le sérum dès les premières minutes de l'HSA et l'effet vasoconstricteur de l'ET-1 est prolongé [47,52]. Il est intéressant de constater que les concentrations d'ET-1 sont élevées au moment même où la production cérébrale de NO est réduite, ce qui accentue encore vraisemblablement les possibilités vasoconstrictrices.…”

Section: Et-1unclassified

Physiopathologie des lésions cérébrales précoces et retardées dans l’hémorragie sous-arachnoïdienne : avancées récentes

Hantson

2011

Réanimation

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MÉDECINPhysiopathologie des lésions cérébrales précoces et retardées dans l'hémorragie sous-arachnoïdienne : avancées récentes* Pathophysiology of acute and delayed brain injury after subarachnoid hemorrhage: an update P. Hantson Reçu le 22 septembre 2011 ; accepté le 10 novembre 2011 © SRLF et Springer-Verlag France 2011Résumé L'hémorragie sous-arachnoïdienne (HSA) par rupture anévrismale est toujours compliquée actuellement d'une mortalité et d'une morbidité importante, qui peuvent être attribuées en grande partie à la survenue de lésions ischémiques précoces ou retardées. Le vasospasme des artères cérébrales est un des facteurs associés aux lésions ischémiques, mais il apparaît avec un certain retard. Les travaux expérimentaux récents s'intéressent aux lésions cérébrales précoces survenant après l'HSA. Plusieurs méca-nismes étiologiques sont proposés : facteurs mécaniques, atteinte de la microcirculation et vasospasme non détectable angiographiquement, perturbation de l'homéostasie ionique, induction de l'apoptose, stress oxydatif… La quantité de sang présente dans les espaces sous-arachnoïdiens déclen-che par ailleurs une riposte inflammatoire qui fait intervenir des éléments cellulaires, mais également des facteurs molé-culaires (cytokines, endothéline, oxyde nitrique [NO]…). Elle est probablement largement responsable des lésions ischémiques retardées dans un contexte de vasospasme. Une meilleure connaissance des mécanismes physiopathologiques impliqués à la phase aiguë devrait permettre de proposer de nouvelles cibles thérapeutiques. Pour citer cette revue : Réanimation 21 (2012). Mots clés Hémorragie sous-arachnoïdienne · Lésions cérébrales précoces et retardées · PhysiopathologieAbstract Aneurysmal subarachnoid hemorrhage (SAH) is still further complicated by a high mortality and morbidity rate related to early or delayed ischemic brain injury. Cerebral vasospasm is one of the factors associated with ischemic injury, but it usually appears with some delay. Recent experimental data are focusing on early brain injury after SAH. Several etiological factors have been suggested: changes in intracranial pressure and cerebral blood flow, microvascular vasospasm and platelet aggregation, cortical spreading depolarization, induction of apoptosis, oxidative stress, etc. The amount of blood present in the subarachnoid space causes an intense inflammatory response that involves both cellular and molecular factors (cytokines, endothelin, nitric oxide) and triggers vasospasm and delayed ischemic neurologic deficit. A better understanding of the pathophysiology of the early brain injury after SAH can lead to a more targeted therapy. To cite this journal: Réanimation 21 (2012).Keywords Subarachnoid hemorrhage · Early and delayed brain injury · Pathophysiology P. Hantson (*) Département des soins intensifs, cliniques Saint-Luc,

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Endothelin-1 levels in plasma and cerebrospinal fluidfollowing subarachnoid haemorrhage

Cited by 11 publications

References 37 publications

Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury

Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury

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

Physiopathologie des lésions cérébrales précoces et retardées dans l’hémorragie sous-arachnoïdienne : avancées récentes

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