Elevated level of endothelin-1 in cerebrospinal fluid and lack of nitric oxide in basilar arterial plasma associated with cerebral vasospasm after subarachnoid haemorrhage in rabbits

Neuschmelting, Volker; Marbacher, Serge; Fathi, Ali-Reza; Jakob, Stephan M.; Fandiño, Javier

doi:10.1007/s00701-009-0350-1

Cited by 25 publications

(18 citation statements)

References 36 publications

(87 reference statements)

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“…The NO levels in plasma and cerebrospinal fluid after SAH have a major impact on the CVS occurrence or not [31,32]. The oxyhemoglobin released from the coagulation in subarachnoid can inhibit eNOS of the adventitia of spasmodic blood vessel and inhibit the synthesis of NO after SAH.…”

Section: Discussionmentioning

confidence: 99%

Influence of Plasma and Cerebrospinal Fluid Levels of Endothelin-1 and No in Reducing Cerebral Vasospasm after Subarachnoid Hemorrhage During Treatment with Mild Hypothermia, in a Dog Model

Wang

Chen

2011

Cell Biochem Biophys

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Using vascular heat-exchange controller implemented mild hypothermia treatment, the authors established the cerebral vasospasm model in which blood was injected twice into dog's foramen magnum; and it was discussed the influence of the concentration of endothelin-1 and NO in blood plasma and cerebrospinal fluid through continuing treatment of mild hypothermia at different times in secondary brain vasospasm model after subarachnoid hemorrhage. Thirty healthy mongrel dogs were randomly divided into five groups; artificial cerebrospinal fluid group (group A), normal temperature control group (group C), mild hypothermia 8 h group (group H1), mild hypothermia 16 h group (group H2), and mild hypothermia 32 h group (group H3). The authors injected the artificial CSF into dog's foramen magnum in group A while the other four groups were injected with autologous arterial blood. The normal group's temperature maintained 38.5°C. The authors set the temperature at 33.5°C in mild hypothermia groups and this was maintained for 8, 16, and 32 h, respectively. ET-1 and NO levels in the cerebrospinal fluid and plasma were assayed in each group on days 0, 7, 14, and 21. Then the changes of the diameter of blood vessels of cerebral basilar artery and overall performance categories score in each group through application of CT angiography were recorded. In the cerebral vasospasm model which was constructed by injecting the blood to dog twice, mild hypothermia treatment, through the application of vascular heat-exchange controller, could reduce cerebral vasospasm. It was observed that the duration of the mild hypothermia is directly proportional to the longer duration of the relieving of cerebral vasospasm. The reciprocal changes observed in the levels of ET-1 and NO in cerebrospinal fluid and plasma revealed that it might be possible to reduce the cerebral vasospasm by regulating the rising amplitude of ET-1 and the decrease in NO in CSF and plasma.

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Section: Discussionmentioning

confidence: 99%

Influence of Plasma and Cerebrospinal Fluid Levels of Endothelin-1 and No in Reducing Cerebral Vasospasm after Subarachnoid Hemorrhage During Treatment with Mild Hypothermia, in a Dog Model

Wang

Chen

2011

Cell Biochem Biophys

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“…In addition, exogenous ET-1 is able to decrease CBF to levels that induce ischemia (Macrae et al, 1993). After both ischemic stroke and SAH, the levels of ET-1 are increased in plasma, cerebrospinal fluid, and cerebral tissue (Lampl et al, 1997;Neuschmelting et al, 2009;Thampatty et al, 2011;Viossat et al, 1993), and although the detected levels are lower than the ones necessary to cause vasoconstriction under normal conditions, increased ET-1 sensitivity of cerebral arteries due to receptor upregulation may allow secreted ET-1 to cause detrimental cerebral vasoconstriction. However, attempts to treat ischemic stroke with specific ET receptor antagonists have produced conflicting results.…”

Section: Ischemic Strokementioning

confidence: 99%

Vascular plasticity in cerebrovascular disorders

Edvinsson

Povlsen

2011

J Cereb Blood Flow Metab

115

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Cerebral ischemia remains a major cause of morbidity and mortality with little advancement in subacute treatment options. This review aims to cover and discuss novel insight obtained during the last decade into plastic changes in the vasoconstrictor receptor profiles of cerebral arteries and microvessels that takes place after different types of stroke. Receptors like the endothelin type B, angiotensin type 1, and 5-hydroxytryptamine type 1B/1D receptors are upregulated in the smooth muscle layer of cerebral arteries after different types of ischemic stroke as well as after subarachnoid hemorrhage, yielding rather dramatic changes in the contractility of the vessels. Some of the signal transduction processes mediating this receptor upregulation have been elucidated. In particular the extracellular regulated kinase 1/2 pathway, which is activated early in the process, has proven to be a promising therapeutic target for prevention of vasoconstrictor receptor upregulation after stroke. Together, those findings provide new perspectives on the pathophysiology of ischemic stroke and point toward a novel way of reducing vasoconstriction, neuronal cell death, and thus neurologic deficits after stroke.

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“…aggregation and vascular tone. This is similar to the wellestablished dichotomy between ET-1 and the vasodilator nitric oxide (NO), where downregulation of NO is potentially accompanied by ET-1 upregulation resulting in vasoconstriction (Neuschmelting et al, 2009). The enzymes on the lipoxygenase side of the eicosanoid pathway are also induced (Alox5, Alox12, Alox15 and Alox5ap), with no previously documented effects by ET-1 directly.…”

Section: Discussionmentioning

confidence: 71%

Endothelin-1-mediated vasoconstriction alters cerebral gene expression in iron homeostasis and eicosanoid metabolism

et al. 2014

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Elevated level of endothelin-1 in cerebrospinal fluid and lack of nitric oxide in basilar arterial plasma associated with cerebral vasospasm after subarachnoid haemorrhage in rabbits

Abstract: This study demonstrates that an elevated ET-1 level in CSF and local lack of NO in the basilar arterial plasma samples are associated with CVS after experimental SAH.

Cited by 25 publications

References 36 publications

Influence of Plasma and Cerebrospinal Fluid Levels of Endothelin-1 and No in Reducing Cerebral Vasospasm after Subarachnoid Hemorrhage During Treatment with Mild Hypothermia, in a Dog Model

Influence of Plasma and Cerebrospinal Fluid Levels of Endothelin-1 and No in Reducing Cerebral Vasospasm after Subarachnoid Hemorrhage During Treatment with Mild Hypothermia, in a Dog Model

Vascular plasticity in cerebrovascular disorders

Endothelin-1-mediated vasoconstriction alters cerebral gene expression in iron homeostasis and eicosanoid metabolism

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