Angiologiia i sosudistaia khirurgiia = Angiology and vascular surgery · 2021
[Vascular, molecular and cellular mechanisms of development of cognitive impairments after occlusion of carotid arteries].
СтатьяНазвание и аннотация: Оригинал на русском
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Guliaev S M
Аннотация
AIM: The study was aimed at determining the role of vascular endothelial dysfunction in induction of molecular and cellular mechanisms of the development of cognitive impairments after occlusion of common carotid arteries.
MATERIAL AND METHODS: The experiments were carried out on Wistar rats. The animals were divided into 2 groups: group 1 - control, sham-operated animals; group 2 - rats with cerebral ischaemia-reperfusion. The model of cerebral ischaemia-reperfusion was reproduced by means of simultaneous occlusion of common carotid arteries (for 5 minutes). The degree of endothelial dysfunction was assessed by determining the amount of circulating endotheliocytes and concentration of nitrogen oxide products in blood plasma. In the brain, we measured the content of malonic dialdehyde, the activity of superoxide dismutase and catalase. Pathomorphological studies of cerebral structures and morphometric analysis of the number of damaged neurons in ischaemic exposure were carried out by means of light microscopy. Cognitive functions in rats were assessed by means of conditioned reaction of passive avoidance and the test of pattern identification.
RESULTS: Common carotid arteries occlusion in rats induced an increase in the level of circulating endotheliocytes and a decrease in end products of nitrogen oxide - nitrites in blood plasma as compared with the control (p≤0.05); the content of malonic dialdehyde in the brain increased 2.6-fold, the activity of superoxide dismutase and catalase decreased 5.9-fold and 2.8-fold, respectively (p≤0.05). The findings of pathomorphological examination registered signs of vasoconstrictive reactions, endothelial oedema, an increase in the proportion of damaged neurons in the cortex of greater hemispheres and hippocampus (p≤0.05). It was determined that occlusion of common carotid arteries in rats resulted in memory disorders revealed in tests of conditioned passive avoidance response and pattern identification (p≤0.05).
CONCLUSION: Occlusion of common carotid arteries in rats becomes a cause of endothelial dysfunction, neurometabolic alterations, damage of neurons in vulnerable regions of the cerebral cortex, hippocampus and cognitive impairments. Damaging factors of the neurovascular system are intensification of oxidative processes and a decrease in the level of antioxidant defence, presenting important targets of neuroprotection.
MATERIAL AND METHODS: The experiments were carried out on Wistar rats. The animals were divided into 2 groups: group 1 - control, sham-operated animals; group 2 - rats with cerebral ischaemia-reperfusion. The model of cerebral ischaemia-reperfusion was reproduced by means of simultaneous occlusion of common carotid arteries (for 5 minutes). The degree of endothelial dysfunction was assessed by determining the amount of circulating endotheliocytes and concentration of nitrogen oxide products in blood plasma. In the brain, we measured the content of malonic dialdehyde, the activity of superoxide dismutase and catalase. Pathomorphological studies of cerebral structures and morphometric analysis of the number of damaged neurons in ischaemic exposure were carried out by means of light microscopy. Cognitive functions in rats were assessed by means of conditioned reaction of passive avoidance and the test of pattern identification.
RESULTS: Common carotid arteries occlusion in rats induced an increase in the level of circulating endotheliocytes and a decrease in end products of nitrogen oxide - nitrites in blood plasma as compared with the control (p≤0.05); the content of malonic dialdehyde in the brain increased 2.6-fold, the activity of superoxide dismutase and catalase decreased 5.9-fold and 2.8-fold, respectively (p≤0.05). The findings of pathomorphological examination registered signs of vasoconstrictive reactions, endothelial oedema, an increase in the proportion of damaged neurons in the cortex of greater hemispheres and hippocampus (p≤0.05). It was determined that occlusion of common carotid arteries in rats resulted in memory disorders revealed in tests of conditioned passive avoidance response and pattern identification (p≤0.05).
CONCLUSION: Occlusion of common carotid arteries in rats becomes a cause of endothelial dysfunction, neurometabolic alterations, damage of neurons in vulnerable regions of the cerebral cortex, hippocampus and cognitive impairments. Damaging factors of the neurovascular system are intensification of oxidative processes and a decrease in the level of antioxidant defence, presenting important targets of neuroprotection.