Treatment of experimental cerebral infarction in rats with levodopa or with glycerol

1978 ◽  
Vol 48 (6) ◽  
pp. 962-969 ◽  
Author(s):  
Pava Popovic ◽  
Vojin Popovic ◽  
Richard Schaffer ◽  
Carl H. Sutton
Keyword(s):  
Cerebral Infarction ◽  
Brain Tissue ◽  
Survival Rates ◽  
Acute Cerebral Infarction ◽  
Pathological Findings ◽  
Carbon Microspheres ◽  
Content Type ◽  
Animal Survival ◽  
Experimental Cerebral Infarction ◽  
Main Factor

✓ Administration of large amounts of levodopa did not improve survival rates of rats after acute cerebral infarction induced by injection of carbon microspheres. However, when 10% glycerol was used, the number of rats that survived after cerebral infarction was significantly greater than in the control or in the levodopa-treated rats. Combination of levodopa and glycerol therapy also significantly improved the survival rate of infarcted animals. It appears that glycerol alone is the main factor in eliciting this beneficial effect. Pathological findings (gross or microscopic) indicate striking changes in brain tissue after embolization. Development of brain edema of the infarcted left hemisphere corresponded to the type of treatment and to the length of animal survival. Brain-tissue histology indicates that glycerol-treated animals developed less severe edema and had less tissue disruption than control animals. The results suggest that treatment of edema should be one of the primary steps in therapy after acute cerebral infarction.

Protective Effect of Paeoniflorin on Acute Cerebral Infarction in Rats

2020 ◽  
Vol 21 (8) ◽  
pp. 702-709
Author(s):  
Weilin Wu ◽  
Chenfeng Qiu ◽  
Xuewen Feng ◽  
Xiaoxiao Tao ◽  
Qian Zhu ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Protective Effect ◽  
Brain Tissue ◽  
Cell Damage ◽  
Acute Cerebral Infarction ◽  
Neurological Deficits ◽  
Sod Activity ◽  
Acute Cerebral Ischemia

Objective: The purpose of this paper was to study the protective effect of paeoniflorin on acute cerebral ischemia. The animal model of cerebral infarction induced by Middle Cerebral Artery Occlusion (MCAO) was blocked by the suture method. Sixty SD rats were randomly divided into the shame group, MCAO group, paeoniflorin (60, 120, 240 mg/kg, respectively) and Nimodipine (NMDP) group (n = 10 per group). Methods: The rats were intragastrically administered immediately after the operation. After 7 days of gavage, the brains were decapitated at 24 h. Hematoxylin and Eosin (HE) staining was used to observe the degree of cell damage in the cerebral cortex of rats. Immunohistochemistry was used to detect silver plating and to observe changes in nerve cells. Rats in the model group showed obvious symptoms of neurological deficits, such as the ischemic morphological changed, the Malondialdehyde (MDA), Lactate Dehydrogenase (LD) content and lactate dehydrogenase (LDH) activity were significantly increased in the ischemic brain tissue, while the Superoxide Dismutase (SOD) activity was decreased. Results: The decrease in Na+-K+-ATPase activity was significantly lower than that in the sham group. The neurological symptoms and signs of MCAO in the different doses of paeoniflorin group were improved, and the neuronal edema in the cortical area was alleviated. The activities of SOD, LDH and Na+-K+-ATPase were significantly increased, and the contents of MDA and LD were decreased. Conclusion: Therefore, paeoniflorin could alleviate the degree of tissue damage in rats with acute cerebral infarction, inhabit the formation of free radicals in the brain tissue after ischemia, and reduce the degree of lipid peroxidation. Thus, the degree of cell damage was reduced greatly and a protective effect was showed on cerebral ischemia.

Ependymal Response in Acute Cerebral Infarction

1974 ◽  
Vol 32 ◽  
pp. 50-51
Author(s):  
Ronald F. Dodson ◽  
Yukio Tagashira
Keyword(s):  
Cerebral Infarction ◽  
Caudate Nucleus ◽  
Brain Tissue ◽  
Squirrel Monkey ◽  
Blood Brain Barrier ◽  
Lateral Ventricle ◽  
Brain Parenchyma ◽  
Acute Cerebral Infarction ◽  
Brain Barrier ◽  
Ependymal Lining

The ependymal complex (subependymal, ependymal, and supraependymal) forms the complex sheath which separates brain parenchyma from ventricular contents. This structure forms a functionally less efficient counterpart to the blood-brain-barrier. That area of the ependymal lining which separates the caudate nucleus from the cavity of the lateral ventricle has recently been described in the adult squirrel monkey. This area was of particular interest since the underlying brain tissue was shown to be of great susceptibility to periods of ischemic as well as hypoxic/ischemic insults.

scholarly journals Evaluation of the Efficacies of Amphotericin B, Posaconazole, Voriconazole, and Anidulafungin in a Murine Disseminated Infection by the Emerging Opportunistic Fungus Sarocladium (Acremonium)kiliense

2013 ◽  
Vol 57 (12) ◽  
pp. 6265-6269 ◽  
Author(s):  
Fabiola Fernández-Silva ◽  
Javier Capilla ◽  
Emilio Mayayo ◽  
Deanna A. Sutton ◽  
Pilar Hernández ◽  
...  
Keyword(s):  
Amphotericin B ◽  
Survival Rates ◽  
Systemic Infection ◽  
Serum Levels ◽  
Antifungal Drugs ◽  
Content Type ◽  
Animal Survival ◽  
Fungal Load ◽  
High Mics

ABSTRACTWe evaluated and compared the efficacies of different antifungal drugs againstSarocladium kiliense(formerlyAcremonium kiliense), a clinically relevant opportunistic fungus, in a murine model of systemic infection. Three clinical strains of this fungus were tested, and the therapy administered was as follows: posaconazole at 20 mg/kg of body weight (twice daily), voriconazole at 40 mg/kg, anidulafungin at 10 mg/kg, or amphotericin B at 0.8 mg/kg. The efficacy was evaluated by prolonged animal survival, tissue burden reduction, and (1→3)-β-d-glucan serum levels. In general, the four antifungal drugs showed high MICs and poorin vitroactivity. The efficacy of the different treatments was only modest, since survival rates were never higher than 40% and no drug was able to reduce fungal load in all the organs for the three strains tested. Posaconazole, in spite of its high MICs (≥16 μg/ml), showed the highest efficacy. The (1→3)-β-d-glucan serum levels were equally reduced by all drugs evaluated.

scholarly journals Repetitive Transcranial Magnetic Stimulation Improves Neuropathy and Oxidative Stress Levels in Rats with Experimental Cerebral Infarction through the Nrf2 Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Hui Liang ◽  
Congjie Xu ◽  
Shijun Hu ◽  
Gang Wen ◽  
Jie Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Infarction ◽  
Reperfusion Injury ◽  
Brain Tissue ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nrf2 Signaling Pathway ◽  
Neuromotor Function ◽  
The Brain ◽  
Experimental Cerebral Infarction

Ischemic stroke poses a serious threat to human health. Its high morbidity, disability, and lethality rates have led to it being a research hotspot. Cerebral ischemia reperfusion injury is a difficult point in the treatment of ischemic stroke. In recent years, studies have shown that repeated transcranial magnetic stimulation (rTMS) can enhance cerebral ischemic tolerance and have a significant protective effect on reperfusion injury after ischemia, but its specific mechanism is unknown. The Nrf2/pathway plays a vital role in ischemia-reperfusion injury in the body environment. Therefore, in this experiment, the middle cerebral artery occlusion (MCAO) reperfusion model of SD rats was made to simulate the occurrence of experimental cerebral infarction by the suture method. After treatment with rTMS, it was studied whether it can regulate the expression of Nrf2 and HO-1, affect the content of MDA and SOD activity, and then activate the Nrf2 pathway to exert its brain protection. The results showed that after MCAO reperfusion, the neurological deficit score of rats increased, and the time to remove the bilateral stickers and the time to cross the balance beam increased, suggesting the successful establishment of the experimental cerebral infarction model. Detecting the brain tissue of experimental cerebral infarction rats found that the expression of Nrf2 and HO-1 decreased, the content of MDA increased, and the activity of SOD decreased. After rTMS treatment, the neuromotor function of experimental cerebral infarction rats improved, the expression of Nrf2 and HO-1 in the brain tissue gradually increased, the content of MDA decreased, and the activity of SOD increased. It indicates that the expression of Nrf2 and HO-1 in experimental cerebral infarction rats is reduced. After treatment with rTMS, it can improve the neuromotor function damage of the rats and reduce the level of oxidative stress. The mechanism may be through promoting the activation of the Nrf2 signaling pathway, acting on the expression of antioxidant proteins, such as HO-1 and SOD1, reducing oxidative stress damage, and playing a protective effect on brain tissue.

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