R. F. Keep

chapter

Aging enhances intracerebral hemorrhage-induced brain injury in rats

Y. Gong, G. H. Xi, R. F. Keep, J. T. Hoff, more

Acta Neurochirurgica Supplements > Intracranial Pressure and Brain Monitoring XII > Experimental aspects > 425-427

Summary Age is an important factor affecting oxidative stress and plasticity after brain injury. The present study investigated the effects of aging on brain injury after intracerebral hemorrhage (ICH). Aging (18- month) and young (3-month) male Sprague-Dawley rats received an intracerebral infusion of 100-µl autologous blood. Age-related changes in brain edema and neurological deficits were examined...

chapter

Intracerebral hemorrhage induces edema and oxidative stress and alters N-methyl-D-aspartate receptor subunits expression

T. Nakamura, R. F. Keep, Y. Hua, J. W. Park, more

Acta Neurochirurgica Supplements > Intracranial Pressure and Brain Monitoring XII > Experimental aspects > 421-424

Summary Intracerebral hemorrhage (ICH) induces brain edema formation via a variety of mechanisms including toxicity due to thrombin and erythrocyte lysis. However, the roles of oxidative damage and excitotoxicity have not been fully elucidated and they are examined in this rat ICH study. Adult male Sprague-Dawley rats received an intracaudate injection of 100 µl autologous whole blood and 5 U of thrombin...

chapter

Ischemia-induced endothelial cell dysfunction

R. F. Keep, A. V. Andjelkovic, S. M. Stamatovic, P. Shakui, more

Acta Neurochirurgica Supplements > Intracranial Pressure and Brain Monitoring XII > Experimental aspects > 399-402

Summary Hemorrhagic transformation upon reperfusion therapy has focused attention on ischemia-induced endothelial dysfunction. This study examined whether hyperglycemia may induce hemorrhagic transformation by enhancing endothelial mitochondrial damage during ischemia and whether preconditioning (PC) stimuli may limit ischemia-induced endothelial damage. In vivo, rats received 2.8 M D-glucose or arabinose...

chapter

Complement inhibition attenuates brain edema and neurological deficits induced by thrombin

Y. Gong, G. H. Xi, R. F. Keep, J. T. Hoff, more

Acta Neurochirurgica Supplements > Intracranial Pressure and Brain Monitoring XII > Experimental aspects > 389-392

Summary The present study examined whether thrombin activates the complement cascade in the brain and whether N-acetylheparin, an inhibitor of complement activation, attenuates brain injury induced by thrombin. There were three sets of studies. In the first set, rats had an intracerebral infusion of either five-unit thrombin or a needle insertion. Brains were sampled at 24 hours for Western blot analysis...

chapter

Systemic use of argatroban reduces tumor mass, attenuates neurological deficits and prolongs survival time in rat glioma models

Y. Hua, L. L. Tang, M. E. Fewel, R. F. Keep, more

Acta Neurochirurgica Supplements > Intracranial Pressure and Brain Monitoring XII > Experimental aspects > 403-406

Summary Our previous studies showed that intracerebral infusion of argatroban, a specific thrombin inhibitor, reduces brain edema and neurological deficits in a C6 glioma model. The present study investigated whether systemic argatroban administration can reduce glioma mass and neurological deficits and extend survival time in C6 and F98 gliomas. Rat C6 or F98 glioma cells were infused into the right...

chapter

Minocycline Attenuates Brain Edema, Brain Atrophy and Neurological Deficits After Intracerebral Hemorrhage

J. Wu, S. Yang, Y. Hua, W. Liu, more

Acta Neurochirurgica Supplements > Brain Edema XIV > Subarachnoid Hemorrhage and Intracerebral Hemorrhage > 147-150

Evidence suggests that microglia activation contributes to brain injury after intracerebral hemorrhage (ICH). The present study aimed to determine if minocycline, an inhibitor of microglia activation, can reduce brain edema, brain atrophy and neurological deficits after ICH. Male Sprague-Dawley rats received an infusion of 100-µL autologous whole blood into the right basal ganglia. Rats received...

chapter

Hyperbaric oxygen preconditioning activates ribosomal protein S6 kinases and reduces brain swelling after intracerebral hemorrhage

Z. Qin, Y. Hua, W. Liu, R. Silbergleit, more

Acta Neurochirurgica Supplements > Acta Neurochirurgica Supplements > Stroke, subarachnoid hemorrhage, and intracerebral hematoma > 317-320

Background New protein synthesis is key to ischemic tolerance induced by preconditioning and ribosomal protein S6 kinases (p70 S6 K) are important enzymes in protein synthesis. Hyperbaric oxygen preconditioning (HBOP) reduces ischemic brain damage. This study investigated if HBOP can activate p70 S6 K and increase new protein synthesis and if HBOP induces brain tolerance against brain swelling...

chapter

Estrogen Reduces Iron-Mediated Brain Edema and Neuronal Death

Y. Gu, G. Xi, W. Liu, R. F. Keep, more

Acta Neurochirurgica Supplements > Brain Edema XIV > Subarachnoid Hemorrhage and Intracerebral Hemorrhage > 159-162

Our previous studies found that 17-β estradiol attenuates edema formation after intracerebral hemorrhage (ICH). As brain iron overload occurs after ICH and contributes to ICH-induced brain injury, the present study examined the effects of estrogen on iron-induced brain injury in vivo and in vitro. There were two sets of experiments in this study. In the first set, male Sprague-Dawley rats were...

article

Effects of intraventricular infusion of vascular endothelial growth factor on cerebral blood flow, edema, and infarct volume

M. R. Harrigan, S. R. Ennis, S. E. Sullivan, R. F. Keep

Acta Neurochirurgica > 2003 > 145 > 1 > 49-53

Background: Therapeutic cerebral angiogenesis, utilizing angiogenic factors to enhance collateral vessel formation within the central nervous system, is a potential method for cerebral revascularization. A prior dose-response study determined that intracerebroventricular infusion of vascular endothelial growth factor (VEGF) increases vascular density with minimal associated brain edema at a concentration...

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Search results for: R. F. Keep

Aging enhances intracerebral hemorrhage-induced brain injury in rats

Intracerebral hemorrhage induces edema and oxidative stress and alters N-methyl-D-aspartate receptor subunits expression

Ischemia-induced endothelial cell dysfunction

Complement inhibition attenuates brain edema and neurological deficits induced by thrombin

Systemic use of argatroban reduces tumor mass, attenuates neurological deficits and prolongs survival time in rat glioma models

Minocycline Attenuates Brain Edema, Brain Atrophy and Neurological Deficits After Intracerebral Hemorrhage

Hyperbaric oxygen preconditioning activates ribosomal protein S6 kinases and reduces brain swelling after intracerebral hemorrhage

Estrogen Reduces Iron-Mediated Brain Edema and Neuronal Death

Effects of intraventricular infusion of vascular endothelial growth factor on cerebral blood flow, edema, and infarct volume

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