Activated oxygen and arachidonate effects on newborn cerebral arterioles

1990 ◽  
Vol 259 (4) ◽  
pp. H1230-H1238 ◽  
Author(s):  
C. W. Leffler ◽  
D. W. Busija ◽  
W. M. Armstead ◽  
D. R. Shanklin ◽  
R. Mirro ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Ultrastructural Changes ◽  
Brain Surface ◽  
Activated Oxygen ◽  
Strong Stimulation ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Direct Generation ◽  
Pial Vessel

We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10(-4) M and 7 x 10(-4) M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.

scholarly journals Effects of Permissive Hypercapnia on Transient Global Cerebral Ischemia–Reperfusion Injury in Rats

2010 ◽  
Vol 112 (2) ◽  
pp. 288-297 ◽  
Author(s):  
Qiang Zhou ◽  
Bo Cao ◽  
Li Niu ◽  
Xiaoguang Cui ◽  
Hongwei Yu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Neurologic Deficit ◽  
Aquaporin 4 ◽  
Global Cerebral Ischemia ◽  
Ultrastructural Changes ◽  
Permissive Hypercapnia ◽  
Group I

Background Permissive hypercapnia is a widely practiced protective ventilatory strategy that has significant protective effects on several models of in vitro and in vivo neuronal injury. However, conclusive effects of permissive hypercapnia on cerebral ischemia are still unknown. Methods One hundred sixty male Wistar rats were divided into five groups: S group (control), ischemia-reperfusion (I/R) group, P1 group, P2 group, and P3 group. I/R was induced by bilateral occlusion of the common carotid arteries, combined with controlled hypotension for 15 min. In groups P1, P2, and P3, the rats inhaled carbon dioxide for 2 h during reperfusion to keep Paco2 within the ranges of 60-80 mmHg, 80-100 mmHg, and 100-120 mmHg, respectively. After 24 and 72 h, neurologic deficit scores, ultrastructural changes, apoptotic neurons, and brain wet-to-dry weight ratios were observed. Caspase-3 and aquaporin-4 protein expression and caspase-3 activity were analyzed. Results Compared with groups I/R and P3, groups P1 and P2 had better neurologic deficit scores and fewer ultrastructural histopathologic changes. I/R-induced cerebral apoptosis was also significantly reduced. The neuroprotective effect was significantly increased in the P2 group compared with the P1 group. There was a significant increase of brain water content and of aquaporin-4 levels in the P3 group. Conclusions Mild to moderate hypercapnia (Paco2 60-100 mmHg) is neuroprotective after transient global cerebral I/R injury. Such a protection might be associated with apoptosis-regulating proteins. In contrast, severe hypercapnia (Paco2 100-120 mmHg) increased brain injury, which may be caused by increased brain edema.

Bardoxolone Ameliorates Cerebral Ischemia/ Reperfusion Injury in Male Rats

2019 ◽  
Vol 22 (04) ◽  
pp. 122-130
Author(s):  
Rihab H Al-Mudhaffer ◽  
Laith M Abbas Al-Huseini ◽  
Saif M Hassan ◽  
Najah R Hadi
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Exploring the Role of Remote Ischemic Preconditioning In Long Term Cognitive Impairment after Global Ischemia-Reperfusion-Induced Vascular Dementia in Mice

2020 ◽  
Author(s):  
Amteshwar Singh Jaggi
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Ischemia ◽  
Vascular Dementia ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
The Brain

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

2020 ◽  
Vol 23 (3) ◽  
pp. 214-224 ◽  
Author(s):  
Esra Cakir ◽  
Ufuk Cakir ◽  
Cuneyt Tayman ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Brain Damage ◽  
Neurological Deficit ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Cortex Cell

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.

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