Impairment of anti-platelet-aggregating activity of endothelial cells after experimental subarachnoid hemorrhage.

Ohkuma, Hiroki; Ogane, Kazumi; Fujita, Shuzo; Manabe, Hiroshi; Suzuki, Shigeharu

doi:10.1161/01.str.24.10.1541

Cited by 33 publications

(16 citation statements)

References 24 publications

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“…Concerning small-vessel lesions, there is little data, but it may be important in conjunction with microcirculation platelet aggregation (194) and vasoreactivity (274). Some possible mechanisms of microvessel constriction have been evoked in a recent review (275).…”

Section: Discussionmentioning

confidence: 99%

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Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

182

140

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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: Discussionmentioning

confidence: 99%

“…Platelet aggregation and adherence to endothelium is one of the known consequences of SAH (194). It certainly stems from the endothelial modifications which occur, but a pattern of specific platelet-derived actions due to the extravasation deserves consideration.…”

Section: -7 Plateletsmentioning

confidence: 99%

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

182

140

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“…6 Moreover, antiplatelet activity of the endothelium is reduced after SAH. 7 Aspirin (acetylsalicylic acid) is a well-known inhibitor of platelet aggregation. 8,9 It also inhibits vasoconstriction mediated through oxyhemoglobin, which is released during lysis of erythrocytes.…”

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confidence: 99%

Antiplatelet Therapy in Aneurysmal Subarachnoid Hemorrhage

Mees

Rinkel

Hop

et al. 2003

Stroke

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Background and Purpose-Observational studies suggest that platelet inhibitors reduce the risk of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage and thereby have a beneficial effect on clinical outcome. Robust evidence, however, is lacking. We performed a systematic meta-analysis to determine whether antiplatelet therapy has a beneficial effect after SAH. Methods-We searched Medline and the Cochrane Library to identify all randomized controlled trials of antiplatelet drugs versus control and calculated relative risks with corresponding 95% confidence intervals (CIs) for poor outcome (dependence or death), the occurrence of DCI, and the occurrence of any intracranial hemorrhage. Results-We included 5 trials totaling 699 patients. The overall relative risk for poor outcome was 0.87 (95% CI, 0.65 to

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“…Preprocedual administration of 300 mg clopidogrel reduced thromboembolic complication in stentassisted coil embolization of ruptured cerebral aneurysms without increasing intracerebral hemorrhage, but after stent deployment integrin inhibitor and 600 mg clopidogrel could not prevent thromboembolic complications in 16% cases 15,18 . An impairment of antiplatelet-aggregating activity has been known to occur in the acute stage of SAH 19 . However, in cases of unruptured aneurysms, the response to preinterventional clopidogrel exhibited great variability and the rate of thromboembolic adverse events related to platelet reactivity was wide-ranging 20 .…”

Section: Acknowledgments and Fundingmentioning

confidence: 99%

Safety of Preprocedural Antiplatelet Medication in Coil Embolization of Ruptured Cerebral Aneurysms at the Acute Stage

et al. 2014

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Preoperative antiplatelet medication for aneurysm coil embolization during acute subarachnoid hemorrhage (SAH) is not common. However, recent advances in neurointerventional devices make antiplatelet medication necessary for SAH surgery. We tested the hypothesis that preprocedural antiplatelet therapy in the acute stage of SAH prevents complications due to ischemia or induced bleeding. We retrospectively reviewed 35 consecutive ruptured cerebral saccular aneurysms that underwent coiling at our institute. Two hundred milligrams of aspirin and 150 mg of clopidogrel were administered to the patients at least two hours before coiling. Systemic heparinization was given after sheath insertion. Procedure-related thrombus formation on digital subtraction angiography, and clinical evidence of ischemia and procedure-related stroke on CT were reviewed. The median patient age was 69 years. Five males and 30 females were included. Seventy-seven percent of patients were Hunt-Hess grades 1 to 3. Assist techniques were used in 20 cases (57%). We inserted one extracranial internal carotid artery stent, but no intracranial stent. Intraoperative thrombosis occurred in one case (2.9%), with no clinical symptoms. Postoperative cerebrospinal fluid drainage was done in three cases, but we experienced no bleeding complications. Preoperative antiplatelet therapy leads to a low rate of thromboembolic events in coiling during acute stage SAH, and this strategy had no adverse influence on bleeding complications.

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Impairment of anti-platelet-aggregating activity of endothelial cells after experimental subarachnoid hemorrhage.

Cited by 33 publications

References 24 publications

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Antiplatelet Therapy in Aneurysmal Subarachnoid Hemorrhage

Safety of Preprocedural Antiplatelet Medication in Coil Embolization of Ruptured Cerebral Aneurysms at the Acute Stage

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