Edema from intracerebral hemorrhage: the role of thrombin

Lee, K. R.; Colón, Gary P.; Betz, A. Lorris; Keep, Richard F.; Kim, Seoung; Hoff, Julian T.

doi:10.3171/jns.1996.84.1.0091

Cited by 331 publications

(216 citation statements)

References 21 publications

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“…The high doses of thrombin (∼20 U) used in previous studies indicating that thrombin can damage dopaminergic neurons in vivo [5,9] are similar to the amount that may be produced by a 100 μL cerebral hemorrhage [26]. The current study, however, indicates that a much smaller dose (1 U) can exacerbate brain injury at the time of 6-OHDA infusion.…”

Section: Discussionmentioning

confidence: 44%

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The effect of thrombin on a 6-hydroxydopamine model of Parkinson's disease depends on timing

Cannon

Hua

Richardson

et al. 2007

Behavioural Brain Research

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Recent results in animal models suggest that thrombin may modulate brain injury in Parkinson's disease (PD). High doses of thrombin (∼20 U) can damage dopaminergic neurons, while we have found that low dose thrombin (1 U), given several days before a brain insult (thrombin preconditioning), is protective in models of PD and stroke. However, the effects of such low levels of thrombin at the time of, or after, exposure to the dopamine neurotoxin 6-hydroxydopamine (6-OHDA) have not been examined and are the focus of this study. In the first set of experiments, rats received co-administration of thrombin (1 U) or saline and 6-OHDA (5 μg) into the medial forebrain bundle. 6-OHDA + thrombin resulted in striking increases in behavioral deficits, compared to 6-OHDA + saline. Similarly, co-administration of an agonist to protease-activated receptor (PAR)-1, a thrombin receptor, also resulted in significantly greater behavioral deficits. In a second set of experiments, thrombin (1 U) or saline was administered 1 or 7 days after 6-OHDA to determine the effects of thrombin after 6-OHDA. Surprisingly, the rats that received saline had strikingly increased behavioral and neurochemical deficits resulting from the 6-OHDA lesion, while delayed thrombin administration prevented this effect. The results indicate that thrombin has differential effects in the

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Section: Discussionmentioning

confidence: 44%

“…Thrombin is a key mediator of edema formation and cell death in experimental stroke [26,37,41]. Recent evidence also suggests that thrombin may modulate brain injury in Parkinson's disease (PD).…”

Section: Introductionmentioning

confidence: 99%

The effect of thrombin on a 6-hydroxydopamine model of Parkinson's disease depends on timing

Cannon

Hua

Richardson

et al. 2007

Behavioural Brain Research

View full text Add to dashboard Cite

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“…At the cellular level, several cell lines, such as neurons, 16,21,23,24,27,29,30 glial/ependymal cells, 26 and endothelium, 25 are known to express receptors for this protein in the CNS. 31 Hoff and coworkers 17,[32][33][34][35][36] studied the effects that blood and its components have on rodent brain tissue and concluded that thrombin induces vasogenic edema as well as direct neurotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Diffusion-Weighted MRI and Proton MR Spectroscopic Imaging in the Study of Secondary Neuronal Injury After Intracerebral Hemorrhage

Carhuapoma

Wang

Beauchamp

et al. 2000

Stroke

113

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Background and Purpose-Cerebral ischemia has been proposed as contributing mechanism to secondary neuronal injury after intracerebral hemorrhage (ICH). Possible tools for investigating this hypothesis are diffusion-weighted (DWI) and proton magnetic resonance spectroscopic imaging ( 1 H-MRSI). However, magnetic field inhomogeneity induced by paramagnetic blood products may prohibit the application of such techniques on perihematoma tissue. We report on the feasibility of DWI and 1 H-MRSI in the study of human ICH and present preliminary data on their contribution to understanding perihematoma tissue functional and metabolic profiles. Methods-Patients with acute supratentorial ICH were prospectively evaluated using DWI and 1 H-MRSI. Obscuration of perihematoma tissue with both sequences was assessed. Obtainable apparent diffusion coefficient (Dav) and lactate spectra in perihematoma brain tissue were recorded and analyzed. Results-Nine patients with mean age of 63.4 (36 to 87) years were enrolled. Mean time from symptom onset to initial MRI was 3.4 (1 to 9) days; mean hematoma volume was 35.4 (5 to 80) cm 3 . Perihematoma diffusion values were attainable in 9 of 9 patients, and 1 H-MRSI measures were obtainable in 5 of 9 cases. Dav in perihematoma regions was 172.5 (120.0 to 302.5)ϫ10Ϫ5 mm 2 /s and 87.6 (76.5 to 102.1)ϫ10 Ϫ5 mm 2 /s in contralateral corresponding regions of interest (Pϭ0.002). One patient showed an additional area of reduced Dav with normal T 2 intensity, which suggests ischemia.1 H-MRSI revealed lactate surrounding the hematoma in 2 patients. Conclusions-DWI and 1 H-MRSI can be used in the study of ICH patients. Our preliminary data are inconsistent with ischemia as the primary mechanism for perihematoma tissue injury. Further investigation with advanced MRI techniques will give a clearer understanding of the role that ischemia plays in tissue injury after ICH. (Stroke. 2000;31:726-732.)

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“…[7][8][9][10][11][12][13][14][15] Recent porcine experiments confirm that intrahematomal heparin can prevent such hyperacute perihematomal edema formation and that intrahematomal tissue plasminogen activator instillation can reduce it. 16 Further supportive human study evidence includes data from a prospective pilot study designed to analyze the effects of thrombocytopathia and/or thrombocytopenia and SICH.…”

Section: Gebel Et Al Natural History Of Perihematomal Edema 2633mentioning

confidence: 99%

Natural History of Perihematomal Edema in Patients With Hyperacute Spontaneous Intracerebral Hemorrhage

Gebel

Jauch

Brott³

et al. 2002

Stroke

215

144

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Background and Purpose-The natural history of perihematomal edema in human hyperacute spontaneous intracerebral hemorrhage (ICH) has not been well described. Methods-This study was a secondary analysis of a previously reported prospective, population-based study of hematoma growth in 142 patients with spontaneous ICH. Patients were first imaged within 3 hours of onset, then 1 and 20 hours later. We excluded patients with anticoagulant use (nϭ7), underlying aneurysm/vascular malformation (nϭ9), trauma (nϭ1), incomplete data (nϭ20), infratentorial ICH (nϭ17), and no consent (nϭ2), leaving an overall study population of 86 patients. From this overall group we further excluded patients with intraventricular extension (nϭ38), subsequent surgery (nϭ5), or death (nϭ2) before 20-hour postbaseline CT. This second, "restricted" analysis group of 41 patients was relatively devoid of clinical or radiological variables likely to confound edema measurement. Absolute and relative edema volumes (edema volume divided by hematoma volume) were descriptively summarized. Correlations between baseline edema volumes and relevant clinical and radiological variables were then performed. Results-Overall, median absolute edema volume increased from 6.93 to 14.4 cm 3 during the first 24 hours after ICH, and median relative edema volume increased from 0.47 to 0.81. In the restricted group, median absolute edema volume was 7.4 cm 3 at baseline and 11.0 cm 3 at 24 hours after ICH, and median relative edema volume increased from 0.55 to 0.81. Baseline relative edema volume was significantly negatively correlated with subsequent change in relative edema volume from baseline to 20-hour CT (rϭ0.57, Pϭ0.0002) but was not significantly correlated with other clinical and radiological variables, including hematoma volume or change in hematoma volume. Conclusions-Perihematomal edema volume increases by approximately 75% during the first 24 hours after hyperacute spontaneous ICH. Patients with the least amounts of baseline relative edema volume were most likely to develop significant additional amounts of edema during the first 24 hours after spontaneous ICH.

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Edema from intracerebral hemorrhage: the role of thrombin

Cited by 331 publications

References 21 publications

The effect of thrombin on a 6-hydroxydopamine model of Parkinson's disease depends on timing

The effect of thrombin on a 6-hydroxydopamine model of Parkinson's disease depends on timing

Diffusion-Weighted MRI and Proton MR Spectroscopic Imaging in the Study of Secondary Neuronal Injury After Intracerebral Hemorrhage

Natural History of Perihematomal Edema in Patients With Hyperacute Spontaneous Intracerebral Hemorrhage

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