Sanguinate's effect on pial arterioles in healthy rats and cerebral oxygen tension after controlled cortical impact

2016 ◽  
Vol 107 ◽  
pp. 83-90 ◽  
Author(s):  
Saad H. Mullah ◽  
Rania Abutarboush ◽  
Paula F. Moon-Massat ◽  
Biswajit K. Saha ◽  
Ashraful Haque ◽  
...  
Keyword(s):  
Oxygen Tension ◽  
Cerebral Oxygen ◽  
Controlled Cortical Impact ◽  
Pial Arterioles ◽  
Cortical Impact

scholarly journals L-Arginine Partially Restores the Diminished CO2 Reactivity after Mild Controlled Cortical Impact Injury in the Adult Rat

2000 ◽  
Vol 20 (5) ◽  
pp. 820-828 ◽  
Author(s):  
Elke M. Golding ◽  
Claudia S. Robertson ◽  
Robert M. Bryan
Keyword(s):  
Polyethylene Glycol ◽  
Free Radical Scavengers ◽  
No Donor ◽  
Controlled Cortical Impact ◽  
Beneficial Effects ◽  
Adult Rat ◽  
Cranial Window ◽  
Pial Arterioles ◽  
Controlled Cortical Impact Injury ◽  
Cortical Impact

Using an open cranial window technique, the authors investigated the mechanisms associated with the suppressed CO2 reactivity after mild controlled cortical impact (CCI) injury in rats. The dilation of arterioles (n = 7) to hypercapnia before injury was 38 ± 12%, which was significantly reduced both at 1 hour (23 ± 15% dilation) and at 2 hours after injury (11 ± 19% dilation). In the presence of L-arginine (10 mmol/L topical suffusion, 300 mg/kg intravenous infusion), the dilation of pial arterioles (n = 6) to hypercapnia was partially restored to 30 ± 6% at 2 hours after injury. In the presence of the nitric oxide (NO) donor, S-nitroso- N-acetylpenicillamine (SNAP) (10−8 mol/L topical suffusion), the dilation of pial arterioles (n = 5) to hypercapnia remained diminished (5 ± 7%) at 2 hours after injury. The dilation of pial arterioles (n = 4) to hypercapnia also remained suppressed (5 ± 6%) with topical suffusion of the free radical scavengers, polyethylene glycol-superoxide dismutase (60 units/mL) and polyethylene glycol-catalase (40 units/mL). The authors have shown that L-arginine at least partially restores the diminished response to hypercapnia after mild CCI injury. Furthermore, these data suggest that the beneficial effects of L-arginine are mediated by a combination of providing substrate for NO synthase and scavenging free radicals.

Segmental Vascular Resistance after Mild Controlled Cortical Impact Injury in the Rat

2003 ◽  
Vol 23 (2) ◽  
pp. 210-218 ◽  
Author(s):  
Elke M. Golding ◽  
Claudia S. Robertson ◽  
Jane C. K. Fitch ◽  
J. Clay Goodman ◽  
Robert M. Bryan
Keyword(s):  
Vascular Resistance ◽  
Controlled Cortical Impact ◽  
Small Vessels ◽  
Cranial Window ◽  
Window Technique ◽  
Pial Arterioles ◽  
Controlled Cortical Impact Injury ◽  
Cortical Impact ◽  
Impact Injury ◽  
The Brain

In an effort to localize the site at which increased resistance occurs after brain trauma, pial arteriole diameter and pressure were assessed after mild controlled cortical impact (CCI) injury in rats using an open cranial window technique. The authors tested the hypothesis that an increase in resistance accompanied by vasoconstriction occurs at the level of the pial arterioles within the injured cortex of the brain. At 1 hour after mild CCI injury, ipsilateral cerebral blood flow was significantly reduced by 42% compared with sham injury (n = 4; P < 0.05). Pial arteriole diameter and pressure remained unchanged. Resistance in the larger arteries (proximal resistance), however, was significantly greater after CCI injury (1.87 ± 0.26 mm Hg/[mL · 100 g · min]) compared with sham injury (0.91 ± 0.21 mm Hg/[mL · 100 g ·min]; P < 0.0001). Resistance in small vessels, arterioles, and venules (distal resistance) was also significantly greater after CCI injury (1.13 ± 0.05 mm Hg/[mL · 100 g · min]) compared with sham injury (0.74 ± 0.13 mm Hg/[mL · 100 g · min]; P = 0.0001). The authors conclude that, at 1 hour after mild CCI injury, changes in vascular resistance comprise a 53% increase in the resistance distal to the area of injury and, surprisingly, a 105% increase in resistance in the arteries proximal to the injury site.

Traumatic Brain Injury-Induced Excitotoxicity Assessed in a Controlled Cortical Impact Model

1993 ◽  
Vol 61 (6) ◽  
pp. 2015-2024 ◽  
Author(s):  
Alan M. Palmer ◽  
Donald W. Marion ◽  
Michelle L. Botscheller ◽  
Pamela E. Swedlow ◽  
Scott D. Styren ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Impact Model ◽  
Controlled Cortical Impact ◽  
Cortical Impact

Acute Response of the Hippocampal Transcriptome Following Mild Traumatic Brain Injury After Controlled Cortical Impact in the Rat

2015 ◽  
Vol 57 (2) ◽  
pp. 282-303 ◽  
Author(s):  
Babru B. Samal ◽  
Cameron K. Waites ◽  
Camila Almeida-Suhett ◽  
Zheng Li ◽  
Ann M. Marini ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Controlled Cortical Impact ◽  
Acute Response ◽  
Cortical Impact

Atorvastatin reduction of intracranial hematoma volume in rats subjected to controlled cortical impact

2004 ◽  
Vol 101 (5) ◽  
pp. 822-825 ◽  
Author(s):  
Dunyue Lu ◽  
Asim Mahmood ◽  
Changsheng Qu ◽  
Anton Goussev ◽  
Mei Lu ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Functional Improvement ◽  
Intracranial Hematoma ◽  
Imaging Device ◽  
Controlled Cortical Impact ◽  
Content Type ◽  
Tissue Sections ◽  
Male Wistar Rats ◽  
Cortical Impact ◽  
Fine Print

Object. Atorvastatin, a β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitor, has pleiotropic effects such as improving thrombogenic profile, promoting angiogenesis, and reducing inflammatory responses and has shown promise in enhancing neurological functional improvement and promoting neuroplasticity in animal models of traumatic brain injury (TBI), stroke, and intracranial hemorrhage. The authors tested the effect of atorvastatin on intracranial hematoma after TBI. Methods. Male Wistar rats were subjected to controlled cortical impact, and atorvastatin (1 mg/kg) was orally administered 1 day after TBI and daily for 7 days thereafter. Rats were killed at 1, 8, and 15 days post-TBI. The temporal profile of intraparenchymal hematoma was measured on brain tissue sections by using a MicroComputer Imaging Device and light microscopy. Conclusions. Data in this study showed that intraparenchymal and intraventricular hemorrhages are present 1 day after TBI and are absorbed at 15 days after TBI. Furthermore, atorvastatin reduces the volume of intracranial hematoma 8 days after TBI.

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