Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage

@article{Gallia2006LeukocyteendothelialCI,
  title={Leukocyte-endothelial cell interactions in chronic vasospasm after subarachnoid hemorrhage},
  author={Gary L. Gallia and Rafael J Tamargo},
  journal={Neurological Research},
  year={2006},
  volume={28},
  pages={750 - 758}
}
Abstract Leukocyte-endothelial cell interactions appear to be the root cause of chronic vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). Early clinical observations and indirect experimental evidence suggested an association between inflammation and chronic vasospasm. Early clinical observations in patients with post-hemorrhagic vasospasm included pyrexia, leukocytosis and the presence of circulating immune complexes. Inflammatory infiltrates and increased levels of immunoglobulins… 
View on Taylor & Francis
ncbi.nlm.nih.gov
69 Citations
Highly Influential Citations
2
Background Citations
27
Methods Citations
1

69 Citations

Citation Type

Citation Type

Role of inflammation (leukocyte-endothelial cell interactions) in vasospasm after subarachnoid hemorrhage.
Inflammation as a Therapeutic Target after Subarachnoid Hemorrhage: Advances and Challenges
TLDR
This chapter provides the current knowledge of the inflammatory response, translational research, and human clinical trials in SAH as well as discusses emerging opportunities for novel therapeutic strategies for clinical management of SAH.
Statins and Anti-Inflammatory Therapies for Subarachnoid Hemorrhage
TLDR
Future directions in the quest to improve outcomes of patients with SAH may need to approach ischemia as a multifactorial process with inflammatory, vasoactive, and ionic/metabolic components.
Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia
TLDR
Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline.
The relationship between IL-6 in CSF and occurrence of vasospasm after subarachnoid hemorrhage.
TLDR
IL-6CSF seems to be a reliable early marker for predicting vasospasm after subarachnoid hemorrhage on Days 3 after treatment before clinical onset, and gender, Hunt & Hess scale (H&H) and Fisher scale of CT after SAH were proved to be the correlation factor with vasospasms.
Cerebrospinal fluid macrophage migration inhibitory factor: a potential predictor of cerebral vasospasm and clinical outcome after aneurysmal subarachnoid hemorrhage.
TLDR
Preliminary evidence from this study suggests that CSF concentrations of MIF are correlated with CV and DCI, however, these results could be confounded in the presence of clinical infection.
Expression of monocyte chemoattractant protein-1 in the cerebral artery after experimental subarachnoid hemorrhage
Inflammation and cerebral vasospasm after subarachnoid hemorrhage.
Depletion of Ly6G/C+ cells ameliorates delayed cerebral vasospasm in subarachnoid hemorrhage
Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH)
TLDR
Current neuroprotective strategies in aSAH are addressed, hopefully leading to future translational therapy options to prevent secondary brain injury in the later phase of disease.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 112 REFERENCES
Prevention of cerebral vasospasm by a humanized anti-CD11/CD18 monoclonal antibody administered after experimental subarachnoid hemorrhage in nonhuman primates.
TLDR
Results show that blockade of leukocyte migration into the subarachnoid space by an anti-CD11/CD18 mAb is effective in preventing experimental cerebral vasospasm in nonhuman primates, despite the unaltered presence of hemoglobin in the subarate space.
Monoclonal antibodies against ICAM-1 and CD18 attenuate cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.
TLDR
These findings provide the first evidence that the severity of cerebral vasospasm can be attenuated using monoclonal antibodies against ICAM-1 and CD18, and suggest that therapeutic targeting of cellular adhesion molecules can be of benefit in treating cerebral Vasospasm.
Cerebrovascular inflammation following subarachnoid hemorrhage.
TLDR
The authors review the available evidence linking factors to the development of inflammatory lesions of the cerebral vasculature and the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-alpha and IL-6.
Endothelial cell expression of intercellular adhesion molecule 1 in experimental posthemorrhagic vasospasm.
TLDR
Endothelial cell ICAM-1 expression seems to be an early and specific signal used by a vessel in response to the deposition of blood periadventitially, and may be a marker for vessels likely to undergo subsequent morphological remodeling and vasospasm.
Prevention of vasospasm by anti-CD11/CD18 monoclonal antibody therapy following subarachnoid hemorrhage in rabbits.
TLDR
Systemic therapy with an anti-CD11/CD18 mAb prevents vasospasm after SAH by inhibiting adhesion of neutrophils and macrophages and their migration into the periadventitial space and supports the concept that leukocyte-endothelial cell interactions play an important role in the pathophysiology of chronic vasosp ASH.
Rise in serum soluble intercellular adhesion molecule-1 levels with vasospasm following aneurysmal subarachnoid hemorrhage.
TLDR
A role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae is suggested as this relationship is further elucidated, adhesion molecules such as ICam-1 may provide novel therapeutic targets in the prevention of vasospasms or itsIschemic consequences.
Monoclonal antibody against E selectin attenuates subarachnoid hemorrhage-induced cerebral vasospasm.
The role of inflammation in experimental cerebral vasospasm.
TLDR
The experiments demonstrate that inflammation alone, in the absence of other processes associated with subarachnoid hemorrhage, may induce persistent and severe cerebroarterial constriction and raises the possibility that inflammation in response to subarACHnoid blood may play a role in clinical vasospasm.
Inflammation in stroke and focal cerebral ischemia.
Inhibition of vasospasm with lymphocyte function-associated antigen-1 monoclonal antibody in a femoral artery model in rats.
TLDR
It is concluded that blocking the migration of inflammatory cells across the endothelial surface of an artery after adventitial exposure to blood prevents the initiation of biological cascades necessary for the subsequent development of chronic vasospasm.
...
1
2
3
4
5
...