Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats

Xi, Guohua; Keep, Richard F.; Hoff, Julian T.

doi:10.3171/jns.1998.89.6.0991

Cited by 304 publications

(240 citation statements)

References 25 publications

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“…For instance, patients with naturally high levels of macrophage/microglial CD163 may have faster rates of hematoma resorption, and/or less neuroinflammation due to rapid sequestration of toxic hemoglobin. In various experimental models of ICH, augmenting hematoma clearance or neutralizing hemoglobin toxicity generally result in less PHE, reduced tissue injury, and improved functional performance in the animals 4, 5, 25, 26…”

Section: Discussionmentioning

confidence: 99%

Soluble CD163 in intracerebral hemorrhage: biomarker for perihematomal edema

Roy-O’Reilly

Zhu

Atadja

et al. 2017

Ann Clin Transl Neurol

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ObjectivePatients with intracerebral hemorrhage (ICH) may elaborate varying degrees of perihematomal edema (PHE), requiring closer monitoring and a higher intensity of treatment. Here, we explore whether the soluble form of CD163, a scavenger receptor responsible for hemoglobin sequestration, can serve as a prognostic biomarker of PHE development and poor outcome after ICH.MethodsOur study cohort was comprised of 51 primary age‐ and sex‐matched ICH patients with moderate‐sized, hypertensive deep hemorrhages. Patients were part of a prospective ICH registry cataloguing admission data along with functional outcomes. We measured sCD163 levels in serial serum and cerebrospinal fluid (CSF) samples obtained at prespecified timepoints. Descriptive statistics, including a generalized estimating equation for longitudinal data, were used to analyze sCD163 in relation to ICH outcomes.ResultsAcute serum sCD163 (<48 h postictus) was significantly elevated in ICH patients compared to both acute neurological event controls (P = <0.001) and healthy controls (P = 0.003). As predicted, acute serum sCD163 levels were significantly associated with both hematoma volume expansion (P = 0.009) and PHE expansion (P = 0.002). Further examination determined that patients with high PHE expansion had poorer modified Rankin Scale scores at discharge (P = 0.024), and circulating sCD163 levels were found to be significantly lower in patients with high‐level PHE expansion.InterpretationAcute sCD163 levels may be a useful biomarker for the acute identification of patients at risk for hematoma expansion, perihematomal edema expansion and poorer short‐term outcomes.

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Section: Discussionmentioning

confidence: 99%

Soluble CD163 in intracerebral hemorrhage: biomarker for perihematomal edema

Roy-O’Reilly

Zhu

Atadja

et al. 2017

Ann Clin Transl Neurol

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“…Packed or lysed RBCs were obtained as previously described. 12 Briefly, autologous blood was washed in saline, and packed RBCs were obtained by centrifugation and discarding the supernatant. Red blood cells were lysed by freezing the packed RBCs in liquid nitrogen (8 minutes) followed by thawing at 371C (5 minutes) three times.…”

Section: Animal Preparation and Intraventricular Injectionmentioning

confidence: 99%

Role of Red Blood Cell Lysis and Iron in Hydrocephalus after Intraventricular Hemorrhage

Gao

Hua

et al. 2014

J Cereb Blood Flow Metab

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118

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Thrombin and iron are two major players in intracerebral hemorrhage-induced brain injury and our recent study found that thrombin contributes to hydrocephalus development in a rat model of intraventricular hemorrhage (IVH). This study investigated the role of red blood cell (RBC) lysis and iron in hydrocephalus after IVH. There were three parts to this study. First, male SpragueDawley rats received an injection of saline, packed, or lysed RBCs into the right lateral ventricle. Second, rats had an intraventricular injection of iron or saline. Third, the rats received intraventricular injection of lysed RBCs mixed with deferoxamine (0.5 mg in 5 mL saline) or saline. All rats underwent magnetic resonance imaging at 24 hours and were then euthanized for brain edema measurement, western blot analysis, or brain histology. We found that intraventricular injection of lysed RBCs, but not packed RBCs, resulted in ventricular enlargement and marked increases in brain heme oxygenase-1 and ferritin at 24 hours. Intraventricular injection of iron also resulted in ventricular enlargement and ventricular wall damage 24 hours later. Coinjection of deferoxamine reduced lysed RBC-induced ventricular enlargement (Po0.01). These results suggest that iron, a degradation product of hemoglobin, has an important role in hydrocephalus development after IVH.

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“…15 Briefly, animals (n ¼ 20) were euthanized, and the brain was removed and dissected into the left and right hemisphere. The cerebellum was kept as an additional control.…”

Section: Histology and Immunohistochemistrymentioning

confidence: 99%

Mouse Intracerebral Hemorrhage Models Produce Different Degrees of Initial and Delayed Damage, Axonal Sprouting, and Recovery

Barratt

Lanman

Carmichael

2014

J Cereb Blood Flow Metab

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The mechanisms of delayed damage and recovery after intracerebral hemorrhage (ICH) remain poorly defined. Two rodent models of ICH are commonly used: injection of the enzyme collagenase (cICH) and injection of autologous blood (bICH). In mice, we compared the effects of these two models on initial and delayed tissue damage, motor system connections, and behavioral recovery. There is no difference in lesion size between models. Injection of autologous blood causes greater mass effect and early mortality. However, cICH produces greater edema, inflammation, and cell death. Injection of the enzyme collagenase causes greater loss of cortical connections and secondary shrinkage of the striatum. Intracerebral hemorrhage occurs within the motor system connections of the striatum. Mapping of the projections of the forelimb motor area shows a significant sprouting in motor cortex projections only in cICH. Both models of ICH produce deficits in forelimb motor control. Behavioral recovery occurs by 5 weeks in cICH and 9 weeks in bICH. In summary, cICH and bICH differ in almost every facet of initial and delayed stroke pathophysiology, with cICH producing greater initial and secondary tissue damage and greater motor system axonal sprouting than bICH. Motor recovery occurs in both models, suggesting that motor system axonal sprouting in cICH is not causally associated with recovery.

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Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats

Abstract: These results demonstrate that RBCs play a potentially important role in delayed edema development after ICH and that RBC lysis and hemoglobin toxicity may be useful targets for therapeutic intervention.

Cited by 304 publications

References 25 publications

Soluble CD163 in intracerebral hemorrhage: biomarker for perihematomal edema

Soluble CD163 in intracerebral hemorrhage: biomarker for perihematomal edema

Role of Red Blood Cell Lysis and Iron in Hydrocephalus after Intraventricular Hemorrhage

Mouse Intracerebral Hemorrhage Models Produce Different Degrees of Initial and Delayed Damage, Axonal Sprouting, and Recovery

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