Βλάβες του εγκεφάλου μετά από αναστολή ερεθισμάτων αρτηριακής πίεσης
Creators: name: Αμανίτη, Αικατερίνη Ν.
Publisher: name: Aristotle University of Thessaloniki
Year: 2007
Subjects: Αορτή
Απονεύρωση
Νευρική καταστροφή
Aorta
Barodenervation
Neural damage

description: Η ρύθμιση της Αρτηριακής Πίεσης περιλαμβάνει πολύπλοκα νευρικά κυκλώματα με συμμετοχή του γλουταμινικού ενώ καταστάσεις όπου η κυκλοφορία σταματά συνοδεύονται από νευρολογικές βλάβες. Σκοπός της παρούσας μελέτης είναι η διερεύνηση πιθανών βλαβών στον εγκέφαλο επίμυων μετά από δικτομή των αορτικών κατασταλτικών νεύρων. 30 άρρενες επίμυες χωρίστηκαν σε δύο ομάδες και υποβλήθηκαν σε αορτική απονεύρωση ή ψευδή επέμβαση υπό συνεχή μέτρηση της αρτηριακής πίεσης. Δύο ώρες μετά το πέρας του πειράματος οι επίμυες θανατώθηκαν. Ο εγκέφαλος παρασκευάσθηκε και εξετάστηκε στο μικροσκόπιο σε συγκεκριμένα επίπεδα που αντιστοιχούν στον κινητικό σωματοαισθητικό φλοιό, ιππόκαμπο, παρεγκεφαλίδα υποθάλαμο και αγκιστρωτά υλικά. Οι επίμυες δεν παρουσίασαν διαφορές ως προς την πίεση ενώ οι απονευρωμένοι επίμυες παρουσίασαν βλάβες στον ιππόκαμπο και κινητικό φλοιό. Η αορτική απονεύρωση συνεπώς πρακαλεί οξεία βλάβη
description: Short-term arterial pressure regulation is under continuous CNS control via complex neural circuits, in order cardiovascular homeostasis to be achieved. Medullary and supramedularry centers are involved in cardiovascular stability. Furthermore, various neurotransmitters have been found to be released in these centers, including glutamate and GABA. On the other hand, excessive glutamate release can induce neuronal damage, caused by mechanisms of excitotoxicity. Aim of the present study was the evaluation of possible acute neuronal damage after barodenervation in rats. 30 male Wistar rats were assigned into two groups to undertake either aortic denervation or Sham operation under continuous blood pressure monitoring. Two hours after completion of the procedure, rats were sacrificed and the brains were dissected, fixed and cut in specific levels, corresponding to dorsomedial hypothalamic nucleus, amygdaloid complex, motor and somatosensory cortex, subregions CA1, CA3 and dentate gyrus of the hippocampus, cingulate cortex and cerebellar Purkinje cells. Sections were stained using hematoxylin and eosin. Sections were examined for dead neurons under light microscope, incorporated with computer image analysis and special software. Groups were compared regarding systolic blood pressure over time, blood pressure variability, absolute number and percentage of dead neurons in the above areas. Statistical analysis was conducted using ANOVA, independent t-test and Mann Whitney U test. Level of significance was set at a&lt;0.05. Groups were comparable regarding systolic blood pressure. Aortic denervated rats showed significant greater blood pressure variability, compared to sham operated rats ((p=0.0284). Dead neurons analysis revealed significant greater number of dead neurons among aortic denervated rats in amygdaloid comlex (p=0.005), motor cortex (p=0.001), layer V of somatosensory cortex (p=0.037), CA1, CA3 and dentate gyrus (p=0.020, p=0.015, p=0.013 respectively) and Purkinje cells (p=0.029). Nevertheless, comparison of percentages of dead neurons between groups showed significant differences only in amygdaloid complex (p=0.002), motor layer (p=0.003 and p=0.000) and subregion CA1 of the hippocampus (p=0.027). Topographic distribution of differential neuronal damage between groups is related to cerebral regions controlling blood pressure. Furthermore, motor cortex and hippocampal CA1 region are considered as the most vulnerable brain regions after hypoxia/iscaemia. This selective vulnerability is attributed to excessive glutamate release under these conditions. In the present study is possible that brain lesions in the same areas are also caused by excessive glutamate release, triggered by aortic denervation. Consecuently, it is also possible that the present study reveal a concurrent mechanism in brain damage after circulatory arrest, provided that circulatory arrest is accompanied by loss of baroreceptor input