[Vascular, molecular and cellular mechanisms of development of cognitive impairments after occlusion of carotid arteries]. / Sosudistye i molekuliarno-kletochnye mekhanizmy razvitiia kognitivnykh rasstroistv posle okkliuzii sonnykh arterii.

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.

[Cognitive impairments and microvascular endothelial dysfunction in unilateral occlusion of the carotid artery]. / Kognitivnye narusheniia i disfunktsiia éndoteliia mikrososudov pri unilateral'noi okkliuzii sonnoi arterii.

OBJECTIVE: The study was aimed at determining cognitive impairments, vascular endothelial dysfunction and morphofunctional alterations of neurons in brain structures (neocortex and hippocampus) in unilateral occlusion of the common carotid artery in albino rats. MATERIAL AND METHODS: The experiments were carried out on Wistar albino rats. The animals were divided into two groups: group 1 - the control group composed of sham-operated rats and group 2 - the study group consisting of rats with cerebral ischaemia. The model of cerebral ischaemia was reproduced by occlusion of the left common carotid artery. Cognitive functions in rats were assessed by means of the object recognition test and conditioned passive avoidance response (CPAR). The degree of vascular endothelial dysfunction was evaluated by the number of circulating endotheliocytes and concentration of end products of nitric oxide - nitrites in blood plasma. Pathomorphological studies of the brain and morphometric analysis of the number of damaged neurons after ischaemic exposure were carried out by means of light microscopy. RESULTS: It was determined that unilateral occlusion of the common carotid artery in rats resulted in memory impairment revealed by the object recognition test and CPAR (p≤0.05). Cerebral ischaemia induced an elevated level of circulating endotheliocytes and a decrease in end products of nitric oxide - nitrates as compared with the controls (p≤0.05). Morphological study demonstrated signs of vasoconstrictive reactions, microvascular endothelial oedema, as well as an increase in the proportion of damaged neurons localized in the fronto-bregmatic region of the cortex of the cerebral hemispheres and hippocampus on the ipsilateral side (p≤0.05). CONCLUSION: Unilateral occlusion of the common carotid artery in albino rats resulted in cognitive impairments, damage of neurons in the most vulnerable areas of the cortex of the cerebral hemispheres and hippocampus predominantly on the ipsilateral side. Cognitive impairments and ischaemic lesions of the brain structures are induced by endothelial dysfunction, enhanced desquamation of endotheliocytes and prevalence of vasoconstrictive reactions resulting from decreased production of the major vasorelaxing factor - nitric oxide.

[Morphological evaluation of cerebroprotective effect of lanthanum acetate in chronic cerebral ischemia in rats].

The objective of this study was to evaluate morphologically the cerebroprotective effect of lanthanum acetate in chronic cerebral ischemia. Chronic cerebral ischemia was reproduced in Wistar rats, weighing 160-180 g, by a ligation of both common carotid arteries. For corection of ischemic cerebral damage, lanthanum acetate (3 mg/kg of body weight, once a day) was introduced intragastrically during the whole experimental period. Ischemic damage of the cerebral cortex was evaluated morphologically in Nissl stained histological sections. Lanthanum acetate was found to suppress the development of ischemia-induced neuronal damage in cerebral hemispheres: the numbers of hyperchromatic neurons, cells with focal chromatolysis, and ghost cells were reduced, while the number of normochromatic neurons was increased in experimental group as compared to those in controls.