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Instytut Medycyny Doświadczalnej i Klinicznej im. M. Mossakowskiego PAN
Contributor:Koźniewska- Kołodziejska, Ewa (Promotor) ; Domin, Helena (Promotor pomocniczy)
Place of publishing: Date issued/created: Description:Bibliografia na str. 92-103 ; 103 s.: il., wykr., tabl., fotogr.; 30 cm.
Degree name: Level of degree: Degree discipline : Degree grantor:Instytut Medycyny Doświadczalnej i Klinicznej im. M. Mossakowskiego PAN
Abstract:Ischemic stroke is one of the major health and socio-economic problems of the aging population of industrialized countries. Despite many years of neuroprotection research and positive results obtained in animal models of stroke, attempts to transfer these potential therapies to the treatment of ischemic stroke patients have failed. However, basic research resulted in some observations that provided a better understanding of the phenomena occurring during acute cerebral ischemia, which were confirmed in human stroke – e.g. attention has been paid to endogenous protective and repair processes occurring in stroke. One of the endogenous substances with potential protective properties is neuropeptide Y (NPY). Activation of Y2 receptors of this neuropeptide has been shown in many in vitro and in vivo studies to reduce the release of excitatory neurotransmitters – the main mediators of excitotoxicity leading to brain cell death after ischemia and in neurodegenerative diseases. The research constituting the foundations of this dissertation aims to explain the basis of the neuroprotective action of the specific agonist of the Y2 receptor – the C-terminal fragment of the neuropeptide Y molecule – NPY(13–36) in vivo, in the model of a middle cerebral artery occlusion with reperfusion (MCAOR), in Sprague-Dawley (SD) normotensive rats and genetically hypertensive rats (SHR). The specific objectives of the study include determining the effect of NPY(13–36) administered to the right lateral ventricle of the brain 30 minutes after the start of ischemia or 30 minutes after the start of reperfusion on: i) the size of the area of the brain damaged by ischemia and reperfusion; ii) selected gait parameters and spontaneous motor activity; iii) microcirculatory response in the ischemic penumbra to an increase in arterial CO2 partial pressure and administration of a nitric oxide synthase inhibitor; iv) the density of the microcirculatory vessels in the penumbra; v) the levelof the leakage of the blood-brain barrier in the ischemic penumbra.The research has shown that NPY(13–36) exerts a beneficial protective effect on the ischemic brain at the microcirculation level in both healthy and hypertensive rats. This effect includes: i) increasing the microflow in the cerebral cortex in the penumbra area during ischemia in SD rats, suggesting recruitment of collateral circulation; ii) reducing the area of post-ischemic brain damage, improving gait parameters, and increasing the density of the smallest vessels of the microcirculation in the cerebral cortex in the penumbra area in both SD and SHR rats 72 hours after brain reperfusion (efficacy when administered in both the ischemia and reperfusion phase); iii) improved microcirculatory response in the penumbra tothe blockade of nitric oxide synthase in SHR rats (efficacy when administered during the reperfusion phase).
Resource type: Detailed Resource Type: Source:IMDiK PAN, sygn. ZS 422 ; click here to follow the link
Language: Language of abstract: Rights:Creative Commons Attribution BY 4.0 license
Terms of use:Copyright-protected material. [CC BY 4.0] May be used within the scope specified in Creative Commons Attribution BY 4.0 license, full text available at: ; -
Digitizing institution:Mossakowski Medical Research Institute PAS
Original in:Library of the Mossakowski Medical Research Institute PAS
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