scholarly journals Effect of Dipyridamole on Cerebral Extracellular Adenosine Level in vivo

1990 ◽  
Vol 10 (3) ◽  
pp. 424-427 ◽  
Author(s):  
T. S. Park ◽  
Jeffrey M. Gidday
Keyword(s):  
Cerebral Ischemia ◽  
Frontal Cortex ◽  
Extracellular Adenosine ◽  
Twofold Increase ◽  
Control Side ◽  
Transport Inhibitor ◽  
Adenosine Concentration ◽  
Brain Dialysis ◽  
Adenosine Transport

The effect of dipyridamole, an adenosine transport inhibitor, on cerebral extracellular adenosine concentration remains to be determined. To examine this issue, bilateral brain dialysis samples were obtained from piglet frontal cortex before, during, and after 5 min of cerebral ischemia; 10−4 M dipyridamole was administered through one dialysis probe. On the control side, dialysate adenosine concentration increased 5.7-fold during ischemia and 15-fold during the first 5 min of reperfusion; it returned to control levels after 15 min of reperfusion. Relative to the control side, dipyridamole caused a twofold increase in basal dialysate adenosine concentration and increased dialysate adenosine concentration at 10 and 15 min of reperfusion, but no increase in dialysate adenosine occurred during and immediately after ischemia. The results indicate that, in the piglet brain, cerebral ischemia markedly elevates intracerebral extracellular adenosine concentration and that dipyridamole increases extracellular adenosine levels.

scholarly journals Increased Brain Interstitial Fluid Adenosine Concentration during Hypoxia in Newborn Piglet

1987 ◽  
Vol 7 (2) ◽  
pp. 178-183 ◽  
Author(s):  
T. S. Park ◽  
David G. L. Van Wylen ◽  
Rafael Rubio ◽  
Robert M. Berne
Keyword(s):  
Frontal Cortex ◽  
Interstitial Fluid ◽  
Acute Hypoxia ◽  
Newborn Piglet ◽  
Cisterna Magna ◽  
Hypoxic Conditions ◽  
Adenosine Concentration ◽  
Brain Dialysis ◽  
The Brain ◽  
Dialysis Technique

The effects of arterial hypoxia on interstitial fluid adenosine concentrations were studied in the frontal cortex and thalamus by the brain dialysis technique and in CSF from the cisterna magna of the newborn piglet. Acute hypoxia (PaO2 = 20 ± 1 mm Hg) increased the interstitial fluid adenosine concentrations significantly from 0.68 ± 0.29 (SEM) to 1.60 ± 0.35 μ M in the frontal cortex and from 1.03 ± 0.32 to 2.60 ± 0.86 μ M in the thalamus (n = 8). Interstitial fluid inosine and hypoxanthine also increased significantly during hypoxia. In separate groups of piglets, the adenosine concentration in the cisterna magna CSF under normoxic conditions was 0.04 ± 0.01 μ M (n = 5), which increased significantly to 0.17 ± 0.04 μ M (n = 6) with hypoxia (PaO2 = 4.7 ± 1.2 mm Hg). Cisterna magna CSF inosine levels did not change significantly during the severe hypoxia. Adenosine concentrations found in the interstitial space and CSF of newborn piglets under normoxic and hypoxic conditions are within the vasodilator range. These results thus suggest that in the neonatal brain adenosine may play a role in regulating blood flow during hypoxia.

Time-lag combination therapy for cerebral ischemia using the FNK protein transduction technology and an immunosuppressant, I: In vivo study

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S57-S57
Author(s):  
Ken-ichiro Kasura ◽  
Megumi Watanabe ◽  
Kumiko Takahashi ◽  
Genki Mizukoshi ◽  
Seiji Ohkubo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Combination Therapy ◽  
Time Lag ◽  
In Vivo Study ◽  
Protein Transduction

scholarly journals Poldip2 controls leukocyte infiltration into the ischemic brain by regulating focal adhesion kinase-mediated VCAM-1 induction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lori N. Eidson ◽  
Qingzeng Gao ◽  
Hongyan Qu ◽  
Daniel S. Kikuchi ◽  
Ana Carolina P. Campos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebral Ischemia ◽  
Focal Adhesion Kinase ◽  
Adhesion Molecules ◽  
Focal Adhesion ◽  
Vascular Inflammation ◽  
Leukocyte Recruitment ◽  
Ischemic Brain ◽  
Inflammatory Monocytes

AbstractStroke is a multiphasic process involving a direct ischemic brain injury which is then exacerbated by the influx of immune cells into the brain tissue. Activation of brain endothelial cells leads to the expression of adhesion molecules such vascular cell adhesion molecule 1 (VCAM-1) on endothelial cells, further increasing leukocyte recruitment. Polymerase δ-interacting protein 2 (Poldip2) promotes brain vascular inflammation and leukocyte recruitment via unknown mechanisms. This study aimed to define the role of Poldip2 in mediating vascular inflammation and leukocyte recruitment following cerebral ischemia. Cerebral ischemia was induced in Poldip2+/+ and Poldip2+/− mice and brains were isolated and processed for flow cytometry or RT-PCR. Cultured rat brain microvascular endothelial cells were used to investigate the effect of Poldip2 depletion on focal adhesion kinase (FAK)-mediated VCAM-1 induction. Poldip2 depletion in vivo attenuated the infiltration of myeloid cells, inflammatory monocytes/macrophages and decreased the induction of adhesion molecules. Focusing on VCAM-1, we demonstrated mechanistically that FAK activation was a critical intermediary in Poldip2-mediated VCAM-1 induction. In conclusion, Poldip2 is an important mediator of endothelial dysfunction and leukocyte recruitment. Thus, Poldip2 could be a therapeutic target to improve morbidity following ischemic stroke.

scholarly journals LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3

Human Cell ◽  
2021 ◽  
Author(s):  
Jiaying Zhu ◽  
Zhu Zhu ◽  
Yipin Ren ◽  
Yukang Dong ◽  
Yaqi Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nuclear Translocation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Mice Model ◽  
Down Regulation

AbstractLINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke.

In vivo exposure to lead does not influence muscarinic receptors in the frontal cortex of the mouse brain

Toxicology ◽  
1994 ◽  
Vol 93 (2-3) ◽  
pp. 99-112 ◽  
Author(s):  
S. Schulte ◽  
W.E. Müller ◽  
K.D. Friedberg
Keyword(s):  
Frontal Cortex ◽  
Mouse Brain ◽  
Muscarinic Receptors
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