Endothelin and aneurysmal subarachnoid haemorrhage: a study of subarachnoid cisternal cerebrospinal fluid.

Gaetani, Paolo; Baena, Riccardo Rodriguez y; Grignani, G; Spanu, G; Pacchiarini, L; Paoletti, P

doi:10.1136/jnnp.57.1.66

Cited by 70 publications

(27 citation statements)

References 34 publications

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“…This discrepancy is all the more difficult to understand since it has been reported that ET antagonists inhibit vasospasm in primates (147,148) as well as in other species. By far the most significant increases of ET concern ET-1, only sporadic amounts of ET-3 being noted in one report (141). However, the precursor, big ET-1, was observed in one study to be the pre-dominant ET in CSF (149).…”

Section: Presence Of Ets In Csf After Sahmentioning

confidence: 99%

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

181

137

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ABSTRACT-Aneurysmal subarachnoid hemorrhage frequently results in complications including intracranial hypertension, rebleeding and vasospasm. The extravasated blood is responsible for a cascade of reactions involving release of various vasoactive and pro-inflammatory factors (several of which are purported to induce vasospasm) from blood and vascular components in the subarachnoid space. The authors review the available evidence linking these factors to the development of inflammatory lesions of the cerebral vasculature, emphasizing: 1) neurogenic inflammation due to massive release of sensory nerve neuropeptides; 2) hemoglobin from lysed erythrocytes, which creates functional lesions of endothelial and smooth muscle cells; 3) activity, expression and metabolites of lipoxygenases cyclooxygenases and nitric oxide synthases; 4) the possible role of endothelin-1 as a pro-inflammatory agent; 5) serotonin, histamine and bradykinin which are especially involved in blood-brain barrier disruption; 6) the prothrombotic and pro-inflammatory action of complement and thrombin towards endothelium; 7) the multiple actions of activated platelets, including platelet-derived growth factor production; 8) the presence of perivascular and intramural macrophages and granulocytes and their interaction with adhesion molecules; 9) the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-a and IL-6. Human and animal studies on the use of anti-inflammatory agents in subarachnoid hemorrhage include superoxide and other radical scavengers, lipid peroxidation inhibitors, iron chelators, NSAIDs, glucocorticoids, and serine protease inhibitors. Many animal studies claim reduced vasospasm, but these effects are not always confirmed in human trials, where symptomatic vasospasm and outcome are the major endpoints. Despite recent work on penetrating vessel constriction, there is a paucity of studies on inflammatory markers in the microcirculation.

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Section: Presence Of Ets In Csf After Sahmentioning

confidence: 99%

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

181

137

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“…A lot of vasoactive compounds have been found in CSF after aneurysm rupture and are supposed to be involved in the pathogenesis of cerebral vasospasm [7,27]: PDGF is released from activated platelets and is considered one of the most potent vasoconstrictor agents [1], but few studies have addressed the question whether PDGF might play a significant role in the pathophysiology of SAH. in the present study we have measured cisternal CSF levels of PDGF in a large series of patients admitted for SAH and addressed the question whether these might be related to the clinical aspects of SAH with special regard for symptomatic vasospasm.…”

Section: Introductionmentioning

confidence: 99%

“…TAT facilitates the gene expression of endothelin 1 [26], the liberation of serotonin and of platelet derived growth factor (PDGF) from platelets: all these events have been related to the pathogenesis of vasospasm [7].…”

Section: Introductionmentioning

confidence: 99%

Platelet derived growth factor and subarachnoid haemorrage: A study on cisternal cerebrospinal fluid

et al. 1997

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Platelet derived growth factor (PDGF) was identified as a powerful mitogenic growth factor which is released from activated platelets and has a marked activity as vasoconstrictor agent. In the present study we have measured cisternal cerebrospinal fluid (CSF) levels of PDGF in 72 patients operated on for intracranial aneurysm in order to verify whether it might be related to the clinical aspects of SAH with special regard to symptomatic vasospasm. CSF samples were obtained at surgery by cisternal puncture of the subarachnoid cistern the nearest to the aneurysm before aneurysm isolation and exclusion. The specimen were frozen in liquid nitrogen and stored at -80 degrees C until analysis. PDGF was measured using a commercially available reagent. Values are expressed as pg/ml of CSF. In 18 cases no radiological and clinical signs of SAH were detected and the mean cisternal CSF level of PDGF was 885.0 +/- 104.5 pg/ml; 20 patients were operated on between day 1 and 3 from the last SAH episode: mean cisternal CSF level of PDGF was 1917.5 +/- 459.4 pg/ml. In 34 patients treated with delayed surgery protocol, mean cisternal CSF level of PDGF was 995.3 +/- 73.8 pg/ml. Statistical analysis showed significant differences between groups (P: 0.011). In the subgroup of patients operated on within day 3 after SAH, 6 presented vasospasm and had mean cisternal CSF PDGF level which was significantly higher (P < 0.01) than in 14 patients without vasospasm. In the delayed "surgical" patients there was no significant difference in cisternal CSF levels of PDGF considering the occurrence of vasospasm. The results of the present study suggest that (a) after SAH there is a significant release of PDGF early after SAH and (b) higher levels of PDGF found in cisternal CSF of patients operated on within 72 hours after SAH may be predictive of symptomatic vasospasm.

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“…Some authors have implicated mechanical factors in development of PTV [34][35][36][37][38], and it is possible that injured vessels release endothelin, a factor that has been implicated in pathogenesis of aneurysmal vasospasm [39,40]. Histologic analysis of cerebral vessels with PTV confirms similarities with aneurysmal vasospasm: tunica intima are thickened, internal elastic lamina are hyper-corrugated, and there are subendothelial connective tissue deposits [13].…”

Section: Posttraumatic Cerebral Artery Vasospasmmentioning

confidence: 78%