Role of blood clot formation on early edema development after experimental intracerebral hemorrhage.

@article{Xi1998RoleOB,
  title={Role of blood clot formation on early edema development after experimental intracerebral hemorrhage.},
  author={G. Xi and K. Wagner and R. Keep and Y. Hua and G. D. de Courten-Myers and J. Broderick and T. Brott and J. Hoff},
  journal={Stroke},
  year={1998},
  volume={29 12},
  pages={
          2580-6
        }
}
BACKGROUND AND PURPOSE Blood "toxicity" is hypothesized to induce edema and brain tissue injury following intracerebral hemorrhage (ICH. [...] Key MethodMETHODS In pigs, we infused autologous blood (with or without heparin) into the cerebral white matter to produce lobar hematomas and froze the brains in situ at 1, 4, or 24 hours after ICH. We determined hematomal and perihematomal edema volumes on coronal sections by computer-assisted morphometry.Expand
Mechanisms of Edema Formation After Intracerebral Hemorrhage: Effects of Extravasated Red Blood Cells on Blood Flow and Blood-Brain Barrier Integrity
TLDR
These results suggest that ischemia is not present at 24 or 72 hours after hematoma induction by injection of intact or lysed RBCs, and RBC constituents that appear after delayed lysis increase blood-brain barrier permeability, which contributes to edema formation. Expand
Complement activation in the brain after experimental intracerebral hemorrhage.
TLDR
It was found that ICH causes complement activation in the brain and blocking the complement cascade could be an important step in the therapy for ICH. Expand
Brain edema after experimental intracerebral hemorrhage: role of hemoglobin degradation products.
TLDR
Limiting hemoglobin degradation coupled with the use of iron chelators may be a novel therapeutic approach to limit brain edema after ICH. Expand
Minor inflammation after surgical evacuation compared with fibrinolytic therapy of experimental intracerebral hemorrhages
TLDR
Despite a significant reduction in hematoma size by surgical removal of the clot, only the inflammatory response, but not the extent of delayed edema can be positively influenced. Expand
Serine protease inhibitor attenuates intracerebral hemorrhage-induced brain injury and edema formation in rat.
TLDR
Systemic administration of FUT reduced brain water content in the ipsilateral basal ganglia 72 h after ICH compared with vehicle and attenuated ICH-induced changes in 8-OHdG and thrombin-reduced brain edema, suggesting that serine protease inhibitor may be potential therapeutic agent for ICH. Expand
Effects of hypothermia on thrombin-induced brain edema formation
TLDR
Inhibition of thrombin-induced BBB breakdown and inflammatory response by hypothermia appear to contribute to brain protection in this model, suggesting hypothermic treatment may provide an approach to potentially reduce ongoing edema after ICH. Expand
Induction of colligin may attenuate brain edema following intracerebral hemorrhage.
TLDR
It is demonstrated that low doses of thrombin upregulate brain colligin levels and attenuate edema formation induced by ICH, and significantly attenuated subsequent ICH-induced brain edema. Expand
Attenuation of intracerebral hemorrhage and thrombin-induced brain edema by overexpression of interleukin-1 receptor antagonist.
TLDR
Overexpression of IL-1ra by using an adenovirus vector attenuated brain edema formation and thrombin-induced intracerebral inflammation following ICH, suggesting that the reduction in ICH-induced edema with IL- 1ra may result from reduction of throm bin-induced brain inflammation. Expand
The role of endogenous versus exogenous tPA on edema formation in murine ICH
TLDR
The role of the endogenous tPA appears to be limited to the early phase of edema formation, whereas exogenous rtPA is edema-promoting between days 3 and 7 after ICH. Expand
Attenuation of thrombin-induced brain edema by cerebral thrombin preconditioning.
TLDR
The phenomenon of thrombin-induced tolerance of the brain to edema formation may be related to HSP27 induction. Expand
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References

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Edema from intracerebral hemorrhage: the role of thrombin.
TLDR
Thrombin plays an important role in edema formation from an intracerebral blood clot, and the edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. Expand
Ultra-early clot aspiration after lysis with tissue plasminogen activator in a porcine model of intracerebral hemorrhage: edema reduction and blood-brain barrier protection.
OBJECT Ultra-early hematoma evacuation (< 4 hours) after intracerebral hemorrhage (ICH) may reduce mass effect and edema development and improve outcome. To test this hypothesis, the authors inducedExpand
Lobar intracerebral hemorrhage model in pigs: rapid edema development in perihematomal white matter.
TLDR
The findings suggest that serum proteins, originating from the hematoma, accumulate in adjacent white matter and result in rapid and prolonged edema after ICH, ie, early perihematomal edema. Expand
Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model.
TLDR
The authors conclude that cell toxicity and BBB disruption by thrombin are triggering mechanisms for the edema formation that follows intracerebral hemorrhage. Expand
Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage.
TLDR
Results demonstrate normal to increased high-energy phosphate and carbohydrate substrate concentrations in edematous perihematomal regions during the early hours following ICH, and speculate that glutamate uptake by astrocytes leads to enhanced aerobic glycolysis and lactate is generated at a rate that exceeds utilization. Expand
Intracerebral infusion of thrombin as a cause of brain edema.
TLDR
It is shown that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/microliter, an amount within the range of concentrations used for topical hemostasis in neurosurgery. Expand
Thrombin may contribute to the pathophysiology of central nervous system injury.
TLDR
Thrombin may play an important role in inflammatory responses to CNS injury since thrombin is one of the blood borne factors that may interact with brain tissue after CNS injury and therapeutic application of antithrombin agents for CNS injury suppresses inflammation and the excessive gliosis and scar formation, which are barriers to neuronal regeneration. Expand
Experimental intracerebral hemorrhage: effects of a temporary mass lesion.
TLDR
Ischemic damage and reduced CBF persisted for 4 hours after transient inflation of a microballoon in the caudate nucleus, suggesting that ischemicDamage occurs at the time of formation of the lesion and is not prevented by its early removal. Expand
Sensitivity and specificity of fluid-blood levels for coagulopathy in acute intracerebral hematomas.
TLDR
Fuid-blood levels in acute intracerebral hemorrhage are moderately sensitive to the presence of coagulopathy (ie, abnormal prothrombin time and partial thromboplastin time) and highly specific for this condition. Expand
Thrombolysis-related intracranial hemorrhage: a radiographic analysis of 244 cases from the GUSTO-1 trial with clinical correlation. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.
TLDR
Although the majority of postthrombolytic ICH are large, solitary, and supratentorial, the spectrum is diverse and features of mass effect reflected the large volumes, and hematoma characteristics of mottling and blood/fluid levels were frequent. Expand
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