Diabetes aggravates heat stress-induced blood-brain barrier breakdown, reduction in cerebral blood flow, edema formation, and brain pathology

Recently, the authors showed that thrombin contributes to the formation of brain edema following intracerebral hemorrhage. The current study examines whether the action of thrombin is due to an effect on cerebral blood flow (CBF), vasoreactivity, blood-brain barrier (BBB) function, or cell viability. In vivo solutions of thrombin were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; CBF and BBB permeability were measured. The actions of thrombin on vasoreactivity were examined in vitro by superfusing thrombin on cortical brain slices while monitoring microvessel diameter with videomicroscopy. In separate experiments C6 glioma cells were exposed to various concentrations of thrombin and lactate dehydrogenase release, a marker of cell death, was measured. The results indicate that thrombin induces BBB disruption as well as death of parenchymal cells, whereas CBF and vasoreactivity are not altered. The authors conclude that cell toxicity and BBB disruption by thrombin are triggering mechanisms for the edema formation that follows intracerebral hemorrhage.

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Anesthetics influence concussive head injury induced blood-brain barrier breakdown, brain edema formation, cerebral blood flow, serotonin levels, brain pathology and functional outcome

International Review of Neurobiology - New Therapeutic Strategies for Brain Edema and Cell Injury ◽

10.1016/bs.irn.2019.06.006 ◽

2019 ◽

pp. 45-81 ◽

Cited By ~ 3

Author(s):

Hari Shanker Sharma ◽

Dafin Fior Muresanu ◽

Ala Nozari ◽

Rudy J. Castellani ◽

Prasanta Kumar Dey ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Head Injury ◽

Functional Outcome ◽

Brain Edema ◽

Blood Brain Barrier ◽

Edema Formation ◽

Barrier Breakdown ◽

Blood Brain Barrier Breakdown ◽

Brain Edema Formation

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Chronic Treatment with Nanoparticles Exacerbate Hyperthermia Induced Blood-Brain Barrier Breakdown, Cognitive Dysfunction and Brain Pathology in the Rat. Neuroprotective Effects of Nanowired-Antioxidant Compound H-290/51

Journal of Nanoscience and Nanotechnology ◽

10.1166/jnn.2009.gr10 ◽

2009 ◽

Vol 9 (8) ◽

pp. 5073-5090 ◽

Cited By ~ 54

Author(s):

Hari Shanker Sharma ◽

Syed F. Ali ◽

Z. Ryan Tian ◽

Saber M. Hussain ◽

John J. Schlager ◽

...

Keyword(s):

Cognitive Dysfunction ◽

Blood Brain Barrier ◽

Chronic Treatment ◽

Brain Barrier ◽

Brain Pathology ◽

Neuroprotective Effects ◽

Blood Brain ◽

Antioxidant Compound ◽

Barrier Breakdown ◽

Blood Brain Barrier Breakdown

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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

Journal of Neurosurgery ◽

10.3171/jns.1997.86.2.0272 ◽

1997 ◽

Vol 86 (2) ◽

pp. 272-278 ◽

Cited By ~ 248

Author(s):

Kevin R. Lee ◽

Nobuyuki Kawai ◽

Seoung Kim ◽

Oren Sagher ◽

Julian T. Hoff

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Intracerebral Hemorrhage ◽

Blood Brain Barrier ◽

Brain Slices ◽

Brain Barrier ◽

C6 Glioma Cells ◽

Edema Formation ◽

Blood Brain

✓ Recently, the authors showed that thrombin contributes to the formation of brain edema following intracerebral hemorrhage. The current study examines whether the action of thrombin is due to an effect on cerebral blood flow (CBF), vasoreactivity, blood-brain barrier (BBB) function, or cell viability. In vivo solutions of thrombin were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; CBF and BBB permeability were measured. The actions of thrombin on vasoreactivity were examined in vitro by superfusing thrombin on cortical brain slices while monitoring microvessel diameter with videomicroscopy. In separate experiments C6 glioma cells were exposed to various concentrations of thrombin, and lactate dehydrogenase release, a marker of cell death, was measured. The results indicate that thrombin induces BBB disruption as well as death of parenchymal cells, whereas CBF and vasoreactivity are not altered. The authors conclude that cell toxicity and BBB disruption by thrombin are triggering mechanisms for the edema formation that follows intracerebral hemorrhage.

Download Full-text