scholarly journals Relation between the Severity of the Sensorimotor Cortical Edema with Cell Swelling and the Duration of Common Carotid Artery Occlusion in Rats (Morphometric Study)

2021 ◽  
Vol 17 (5) ◽  
pp. 111-128
Author(s):  
S. S. Stepanov ◽  
D. V. Avdeev ◽  
V. A. Akulinin ◽  
A. Yu. Shoronova ◽  
L. M. Makarieva ◽  
...  

The aim of the study. To examine the changes in structure and morphometry in sensorimotor cortical edema with cell swelling in mature white rats after common carotid artery occlusion of various durations.Material and methods. Acute ischemia was modeled on white adult Wistar rats by 20-, 30- and 40-min occlusion of the common carotid arteries (CCA). Histological (hematoxylin-eosin and Nissl staining), immunohistochemical (NSE, MAP-2, GFAP) and morphometric methods were used. Morphometry was assessed on hematoxylin and eosin-stained specimens using ImageJ 1.53 plug-ins (Find Maxima, Find Foci). Statistical hypothesis testing (nonparametric criteria) was performed using Statistica 8.0 software.Results. In the sensorimotor cortex (SMC) of white rats after 20, 30 and 40 minutes of CCA occlusion the signs of cytotoxic brain edema appeared, focal destructive and adaptive changes of neurons and astroglia evolved. The edema persisted throughout the observation period (7 days). The increase in the relative area, the number of cell swelling zones and their hydration (pixel brightness) was significant. On days 1 and 3 after CCA occlusion, some of the SMC astrocyte processes underwent destruction. Subpial and perivascular zones suffered to a greater extent. Mild and moderate (after unilateral 30-min CCA occlusion) to moderate and severe (after bilateral 40-min CCA occlusion) scattered structural and functional changes of the SMC with large areas of clearing in the «porous» neuropil, severe perivascular and perineuronal edema of the astrocyte processes developed. The latter was associated with a moderate reduction of the total neuronal density.Conclusion. After occlusion of CCA, signs of edema with cellular swelling appeared in the SMC amid dystrophic and necrotic pyramidal neurons and activated neuroglial cells. To a greater extent, the signs of brain swelling were evident three days after bilateral 40-min occlusion of CCA.

2021 ◽  
Vol 14 (3) ◽  
pp. 223
Author(s):  
Deokho Lee ◽  
Yohei Tomita ◽  
Yukihiro Miwa ◽  
Heonuk Jeong ◽  
Kiwako Mori ◽  
...  

Ocular ischemia is a common cause of blindness and plays a detrimental role in various diseases such as diabetic retinopathy, occlusion of central retinal arteries, and ocular ischemic syndrome. Abnormalities of neuronal activities in the eye occur under ocular ischemic conditions. Therefore, protecting their activities may prevent vision loss. Previously, peroxisome proliferator-activated receptor alpha (PPARα) agonists were suggested as promising drugs in ocular ischemia. However, the potential therapeutic roles of PPARα agonists in ocular ischemia are still unknown. Thus, we attempted to unravel systemic and ocular changes by treatment of fenofibrate, a well-known PPARα agonist, in a new murine model of ocular ischemia. Adult mice were orally administered fenofibrate (60 mg/kg) for 4 days once a day, followed by induction of ocular ischemia by unilateral common carotid artery occlusion (UCCAO). After UCCAO, fenofibrate was continuously supplied to mice once every 2 days during the experiment period. Electroretinography was performed to measure retinal functional changes. Furthermore, samples from the retina, liver, and blood were subjected to qPCR, Western blot, or ELISA analysis. We found that fenofibrate boosted liver function, increased serum levels of fibroblast growth factor 21 (FGF21), one of the neuroprotective molecules in the central nervous system, and protected against UCCAO-induced retinal dysfunction. Our current data suggest a promising fenofibrate therapy in ischemic retinopathies.


PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11665
Author(s):  
Deokho Lee ◽  
Heonuk Jeong ◽  
Yukihiro Miwa ◽  
Ari Shinojima ◽  
Yusaku Katada ◽  
...  

Background Retinal ischemic stresses are associated with the pathogenesis of various retinal vascular diseases. To investigate pathological mechanisms of retinal ischemia, reproducible, robust and clinically significant experimental rodent models are highly needed. Previously, we established a stable murine model of chronic hypoperfusion retinal injuries by permanent unilateral common carotid artery occlusion (UCCAO) and demonstrated chronic pathological processes in the ischemic retina after the occlusion; however, retinal functional deficits and other acute retinal ischemic injuries by UCCAO still remain obscure. In this study, we attempted to examine retinal functional changes as well as acute retinal ischemic alterations such as retinal thinning, gliosis and cell death after UCCAO. Methods Adult mice (male C57BL/6, 6–8 weeks old) were subjected to UCCAO in the right side, and retinal function was primarily measured using electroretinography for 14 days after the surgery. Furthermore, retinal thinning, gliosis and cell death were investigated using optical coherence tomography, immunohistochemistry and TUNEL assay, respectively. Results Functional deficits in the unilateral right retina started to be seen 7 days after the occlusion. Specifically, the amplitude of b-wave dramatically decreased while that of a-wave was slightly affected. 14 days after the occlusion, the amplitudes of both waves and oscillatory potentials were significantly detected decreased in the unilateral right retina. Even though a change in retinal thickness was not dramatically observed among all the eyes, retinal gliosis and cell death in the unilateral right retina were substantially observed after UCCAO. Conclusions Along with previous retinal ischemic results in this model, UCCAO can stimulate retinal ischemia leading to functional, morphological and molecular changes in the retina. This model can be useful for the investigation of pathological mechanisms for human ischemic retinopathies and furthermore can be utilized to test new drugs for various ischemic ocular diseases.


2013 ◽  
Vol 58 (3) ◽  
pp. 846 ◽  
Author(s):  
C. Klonaris ◽  
G.N. Kouvelos ◽  
M. Kafeza ◽  
A. Koutsoumpelis ◽  
A. Katsargyris ◽  
...  

Author(s):  
Julie Kromm ◽  
Tim E. Darsaut ◽  
Khurshid Khan ◽  
Robert Ashforth ◽  
Esseddeeg Ghrooda

AbstractAlthough the common carotid artery is the second most common site for extracranial carotid artery stenosis, complete symptomatic occlusion in the absence of devastating stroke is rare. We present a case of complete common carotid artery occlusion failing medical management and requiring endovascular intervention. The clinical presentation, diagnostic investigations, and management of complete carotid artery occlusions are discussed.


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