Immunological Study of Late Cerebral Vasospasm in Subarachnoid Hemorrhage

Hoshi, Taeko; Shimizu, Takashi; Kito, Kenichi; Yamasaki, Nobuhiko; Takahashi, Kenji; Takahashi, Masako; Okada, Takaharu; Kasuya, Hidetoshi; Kitamura, Koichi

doi:10.2176/nmc.24.647

Cited by 61 publications

(7 citation statements)

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“…Argatroban administered 1 h after ICH rapidly reduced the infiltration of PMNs, which indicated that the thrombin inhibitor could be promising even if administered afterwards, as indicated by Kitaoka et al [9]. Other functions of thrombin including direct cell toxicity [11], cytokine release [14, 15, 16, 17], regulation of neutrophil adhesion to endothelia [18, 19], and platelet aggregation [16, 20]might have an effect on the edema, although we did not evaluate this.…”

Section: Discussionmentioning

confidence: 99%

Systemic Administration of Argatroban Reduces Secondary Brain Damage in a Rat Model of Intracerebral Hemorrhage: Histopathological Assessment

Nagatsuna

Nomura²,

Suehiro³

et al. 2005

Cerebrovasc Dis

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This study investigated the effects of argatroban, a thrombin inhibitor, on brain edema and inflammation in a rat intracerebral hemorrhage (ICH) model. ICH was induced by injecting collagenase IV into the right caudate nucleus. Argatroban was administered intraperitoneally. Argatroban reduced brain edema from 44.6 to 14.3 µl at 72 h. Infiltration of polymorphonuclear leukocytes at 24 h and monocyte/macrophage at 24 and 72 h was significantly suppressed by argatroban. Argatroban did not increase the volume of hematoma. Systemic administration of argatroban reduced secondary brain damage including edema and inflammation in a rat ICH model.

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Section: Discussionmentioning

confidence: 99%

Systemic Administration of Argatroban Reduces Secondary Brain Damage in a Rat Model of Intracerebral Hemorrhage: Histopathological Assessment

Nagatsuna

Nomura²,

Suehiro³

et al. 2005

Cerebrovasc Dis

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“…Experimental and clinical evidence suggests that Intercellular Adhesion Molecule 1 (ICAM-1) mediated leukocyte migration may play a crucial role in the patho-genesis of cerebral vasospasm [9][10][11][12][13]. SAH increases endothelial ICAM-1 expression [1,[3][4][5]26,27] and resultant perivascular leukocyte migration [1,[3][4][5]9,14,15].…”

Section: Discussionmentioning

confidence: 99%

“…Identifying risk factors may improve clinical prediction and allow for more effective treatment of vasospasm. The measurement of sensitive inflammatory markers such as CRP significantly increases our ability to predict with accuracy and prevent or appropriately treat coronary thrombotic events [10][11][12][13]. Previous clinical studies have shown that elevated levels of high-sensitivity CRP could predict the development of coronary vasospasm [8,9].…”

Section: Introductionmentioning

confidence: 99%

Predicting vasospasm after aneurismal subarachnoid hemorrhage with C reactive protein levels

Romero¹,

Ducati²,

Zanini³

et al. 2013

Health

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Aim: The interest of inflammatory marker increased in the last years, even in preventing clinical outcome after subarachnoid hemorrhage (SAH). Our objective was to study the relationships between C-reactive protein levels and clinical outcome and the development of cerebral vasospasm after aneurismal SAH. Methods: One hundred adult patients with aneurismal SAH were prospectively evaluated. Glasgow Coma Scale (GCS) score, Hunt and Hess grade, Fisher grade, CT scans, digital subtraction angiography studies, transcranial doppler (TCD) and daily neurological examinations were recorded. Serial serum CRP measurements were obtained on daily between admission and 10th days. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to predict outcome. Results: A progressive increase in the CRP levels from the admission to the 3rd postictal day was observed, followed by a slow decrease until the 9th day. Hemodynamic changes in TCD were associated with higher serum CRP levels. Patients with lower GCS scores presented with increased CRP levels. Patients with higher Hunt and Hess grades on admission developed significantly higher CRP serum levels. Patients with higher admission Fisher grades showed increased levels of CRP. A statistically significant inverse correlation was established in our series between CRP serum levels and GOS and mRS scores on discharge and CRP levels. Conclusion: Increased CRP levels were strongly associated with poor clinical outcome. CRP levels can predict cerebral vasospasm and delayed ischemic deficits with higher statistic significance. There are relationships between hemodynamic chances in TCD and higher CRP levels.

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“…Early studies noted that aSAH patients with vasospasm had higher white blood cell counts, complement activation, and circulating immune complexes than patients without vasospasm [135][136][137][138]. Histopathologic examinations have shown lymphocyte, macrophage, and granulocyte infiltration as well as immunoglobulin and complement deposits in the vessel walls [139,140]. Since these early observations, there has been mounting evidence that vasospasm is a manifestation of a pathologic, biphasic inflammatory response.…”

Section: Vasospasm/sahmentioning

confidence: 99%

The potential for immune checkpoint modulators in cerebrovascular injury and inflammation

Kim

Patel

Jackson

2021

Expert Opinion on Therapeutic Targets

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Introduction: Neuroinflammation has been linked to poor neurologic and functional outcomes in many cerebrovascular disorders. Immune checkpoints are upregulated in the setting of traumatic brain injury, intracerebral hemorrhage, ischemic stroke, central nervous systems vasculitis, and post-hemorrhagic vasospasm, and are potential mediators of pathologic inflammation. Burgeoning evidence suggests that immune checkpoint modulation is a promising treatment strategy to decrease immune cell recruitment, cytokine secretion, brain edema, and neurodegeneration. Areas covered: This review discusses the role of immune checkpoints in neuroinflammation, and the potential for therapeutic immune checkpoint modulation in inflammatory cerebrovascular disorders. A search of Pubmed and clinicaltrials.gov was performed to find relevant literature published within the last 50 years. Expert opinion: The clinical success of immune-activating checkpoint modulators in human cancers has shown the immense clinical potential of checkpoint-based immunotherapy. Given that checkpoint blockade can also precipitate a pathologic pro-inflammatory or autoimmune response, it is plausible that these pathways may also be targeted to quell aberrant inflammation. A limited but growing number of studies suggest that immune checkpoints play a critical role in regulating the immune response in the central nervous system in a variety of contexts, and that immune-deactivating checkpoint modulators may be a promising treatment strategy for acute and chronic neuroinflammation in cerebrovascular disorders.

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Immunological Study of Late Cerebral Vasospasm in Subarachnoid Hemorrhage

Cited by 61 publications

References 0 publications

Systemic Administration of Argatroban Reduces Secondary Brain Damage in a Rat Model of Intracerebral Hemorrhage: Histopathological Assessment

Systemic Administration of Argatroban Reduces Secondary Brain Damage in a Rat Model of Intracerebral Hemorrhage: Histopathological Assessment

Predicting vasospasm after aneurismal subarachnoid hemorrhage with C reactive protein levels

The potential for immune checkpoint modulators in cerebrovascular injury and inflammation

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