Endothelin in plasma and cerebrospinal fluid of patients with subarachnoid haemorrhage

Fujimori, A.; Yanagisawa, Masashi; Saito, Akira; Goto, Katsutoshi; Takao, Masaki; Mima, Tatsuya; Takakura, Kintomo; Shigeno, Taku

doi:10.1016/0140-6736(90)93432-o

Cited by 121 publications

(56 citation statements)

References 6 publications

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“…The ET-1 levels in the perivascular space and in the cisternal CSF were high enough to produce vasospasm; [3,25,47] however, the levels were unchanged by the development or resolution of vasospasm. These results indicate that the increase in CSF ET-1 levels observed by others [11,14,48,49] cannot be solely responsible for the development of vasospasm. On the other hand, if oxyhemoglobin, an agent purportedly responsible for vasospasm, [31,46] eliminates the action of vasodilatory agent(s), [18,22,43,52] then vasospasm could result from the unopposed action of a constricting agent like ET-1.…”

Section: Vasospasm and Et-1mentioning

confidence: 49%

“…[11,48] Our results suggest that the increased CSF ET-1 levels observed in patients after rupture of an intracranial aneurysm and in patients with clinical symptoms of vasospasm [11,14,48,49] are not solely responsible for the development of vasospasm; rather, they result from ischemia occurring after SAH.…”

Section: Source and Cause Of Et-1 Presence In Csf After Intracranial mentioning

confidence: 86%

“…[9,11,14,19,24,33,37,40,[47][48][49] This controversial [5,19] hypothesis is supported by a delayed onset of long-lasting spasm of the intracranial vessels produced by intracisternal administration of ET-1, [3,47] by an increase in ET-1 levels in CSF after SAH in humans, [11,14,48,49] and by a decrease in the incidence of vasospasm after use of ET-1 receptor antagonists. [8,23,34,38,57] Astrocytes, neurons, and pituitary cells produce ET-1.…”

Section: Discussionmentioning

confidence: 99%

“…[31,46] One of the potential oxyhemoglobin-related mechanisms of vasospasm is the release of endothelin-1 (ET-1), [3,33,37] a potent endothelium-derived vasoconstricting agent, [21,55] into the cerebrospinal fluid (CSF) after SAH. [3,11,14,15,19,21,25,33,[47][48][49] Not only are astrocytes, neurons, and pituitary cells a normal source of extraluminal ET-1, [10,17,26,29,56] but endothelial [9,24,40] and smooth-muscle [24] cells also release ET-1 when stimulated by oxyhemoglobin [9,24,40] or thrombin. [10 ] Because an increase in the levels of ET-1 in CSF has been described in patients with cerebral vasospasm and delayed ischemic neurological deficits after SAH, [11,14,48,49] the production of ET-1 may also be induced by ischemia.…”

mentioning

confidence: 99%

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Source and cause of endothelin-1 release to cerebrospinal fluid after subarachnoid hemorrhage

Pagnanelli

Barrer²

1997

FOC

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Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of experiments. In a primate model of SAH, serial ET-1 levels were measured in samples from the perivascular space by using a microdialysis technique and in cerebrospinal fluid (CSF) and plasma during the development and resolution of delayed vasospasm. To determine whether elevated ET-1 production was a direct cause of vasospasm or acted secondary to ischemia, the authors also measured ET-1 levels in plasma and CSF after transient cerebral ischemia. To elucidate the source of ET-1, they measured its production in cultures of endothelial cells and astrocytes exposed to oxyhemoglobin (10 μM), methemoglobin (10 μM), or hypoxia (11% oxygen). There was no correlation between the perivascular levels of ET-1 and the development of vasospasm or its resolution. Cerebrospinal fluid and plasma levels of ET-1 were not affected by vasospasm (CSF ET-1 levels were 9.3 ± 2.2 pg/ml and ET-1 plasma levels were 1.2 ± 0.6 pg/ml) before SAH and remained unchanged when vasospasm developed (7.1 ± 1.7 pg/ml in CSF and 2.7 ± 1.5 pg/ml in plasma). Transient cerebral ischemia evoked an increase of ET-1 levels in CSF (1 ± 0.4 pg/ml at the occlusion vs. 3.1 ± 0.6 pg/ml 4 hours after reperfusion; p < 0.05), which returned to normal (0.7 ± 0.3 pg/ml) after 24 hours. Endothelial cells and astrocytes in culture showed inhibition of ET-1 production 6 hours after exposure to hemoglobins. Hypoxia inhibited ET-1 release by endothelial cells at 24 hours (6.4 ± 0.8 pg/ml vs. 0.1 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05) and at 48 hours (6.4 ± 0.6 pg/ml vs. 0 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05), but in astrocytes hypoxia induced an increase of ET-1 at 6 hours (1.5 ± 0.6 vs. 6.4 ± 1.1 pg/ml, control vs. hypoxic astrocytes; p < 0.05). Endothelin-1 is released from astrocytes, but not endothelial cells, during hypoxia and is released from the brain after transient ischemia. There is no relationship between ET-1 and vasospasm in vivo or between ET-1 and oxyhemoglobin, a putative agent of vasospasm, in vitro. The increase in ET-1 levels in CSF after SAH from a ruptured intracranial aneurysm appears to be the result of cerebral ischemia rather than reflecting the cause of cerebral vasospasm.

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Section: Vasospasm and Et-1mentioning

confidence: 49%

Section: Source and Cause Of Et-1 Presence In Csf After Intracranial mentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Source and cause of endothelin-1 release to cerebrospinal fluid after subarachnoid hemorrhage

Pagnanelli

Barrer²

1997

FOC

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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

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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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Endothelin-induced protein tyrosine phosphorylation of cultured astrocytes: Its relationship to cytoskeletal actin organization

Kōyama¹,

Baba²

1999

Glia

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Endothelin in plasma and cerebrospinal fluid of patients with subarachnoid haemorrhage

Cited by 121 publications

References 6 publications

Source and cause of endothelin-1 release to cerebrospinal fluid after subarachnoid hemorrhage

Source and cause of endothelin-1 release to cerebrospinal fluid after subarachnoid hemorrhage

Molecular Pharmacology and Pathophysiological Significance of Endothelin

Endothelin-induced protein tyrosine phosphorylation of cultured astrocytes: Its relationship to cytoskeletal actin organization

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