Konvülziyonlar ve akut hipertansiyonda kan-beyin bariyeri yıkımına etkili faktörler
Başlık çevirisi mevcut değil.
- Tez No: 111643
- Danışmanlar: PROF.DR. BARİA ÖZTAŞ
- Tez Türü: Doktora
- Konular: Fizyoloji, Physiology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 1993
- Dil: Türkçe
- Üniversite: İstanbul Üniversitesi
- Enstitü: Sağlık Bilimleri Enstitüsü
- Ana Bilim Dalı: Fizyoloji Ana Bilim Dalı
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 75
Özet
¦53- ÖZET Konvülziyonlarda ve akut hipertansiyonda, kan-beyin bariyeri permeabilitesinın artmasında; arteryel hipertansiyonun, ZİP nin ve hipoperfüzyonun rolünü aydınlatmak için aşağıdaki deneyler ve deney grupları plânlandı. A-Kontrol Grubu (n=10) B-Konvulziyon Grubu 1- Pentilentetrazol konvulziyonu (n=14) 2- iki taraflı a.karotis kommunis bağlı pentilentetrazol konvulziyonu (n=10) 3- A.karotis kommunis hemen açılıp pentilentetrazol konvul ziyonu oluşturulan grup (reperfüze grubu) (n=12) 4-Pentilentetrazol ile kan basıncı yükseltilip GABA ile kan basıncının hemen düşürüldüğü AP Grubu ( JP=Maksimal kan basıncı- kontrol kan basıncı) (n=12) C-Akut Hipertansiyon Grubu 1-Akut adrenalin hipertansiyonu (n=17) 2-Akut adrenalin hipertansiyonu oluşturulup, bir Ca-antagonisti olan nifedipin ile hemen kan basıncının düşürüldüğü AP grubu (n-7).-54- 3. Sağ a.karotis kommunis 3 saat süreyle bağlandıktan sonra, belli sürelerle reperfüzyon yapılıp, adrenalin hipertansiyonu oluş turulan gruplar; a-5 dak. reperfüzyon + adrenalin hipertansiyonu (n=ll) b-30 dak. reperfüzyon + adrenalin hipertansiyonu (n=10) c-180 dak. reperfüzyon + adrenalin hipertansiyonu (n=10) d-5.,30.,180.dak.reperfüzyondan sonra adrenalin hipertansiyonu yapılmadan Evans-blue albumin ekstravazasyonunun incelendiği gruplar (Her grup için n=10). Bu amaçla; pentilentetrazol konvulziyonl arında; iki taraflı a.karotis kommunis bağlı iken ve reperfüzyon fazında oluşturulan konvulziyonlardaki kan-beyin bariyeri yıkımları hem makroskopik olarak Rapoport kriterlerine göre, hem de kantitatif olarak spektrofo tometrik değerlerle tespit edildi. 80 mgr/kg Pentilentetrazol vererek generalize nöbetler oluş turduğumuz hayvanların %92 nin kan-beyin bariyeri permeabilitesinde artış görüldü. Bu permeabilite artışları; genellikle talamus,hıpo talamuS,Substansia nigra, korpus striatum ve medulla oblangatada göz lendi. Aynı deney koşullarında spektrofotometrik tayinlerde Evans-blue kon santrasyonu bu grupta 1.040+0.321 mgr.% olarak bulundu. İki taraflı a.karotis kommunis bağlı grupta 7 hayvanda +1 yıkım tespit edildi. Yıkım alanları genellikle korteks bölgelerin- deydi. Bu yedi hayvanın 3 tanesinin talamus çekirdeklerinde de yıkım vardı. Spektrofotometrik yöntemle Evans-blue konsantrasyonu bu grup ta 0.549+0.121 mgr.% ye kadar azaldı. Pentilentetrazol nöbetleri ile, iki taraflı a.karotis kommunis bağlı iken meydana gelen nöbetler deki bariyer yıkımları arasındaki fark anlamlı bulundu (p
Özet (Çeviri)
-57- SUMMARY Experiments were made in order to elucidate the role of arterial hypertension, AP and hypoperfusion in increased blood-brain barrier permeability in convulsions and acute hypertension and the following experimental groups were planned. A-Control Group (n=10) B-Convulsion Groups 1-Convulsion induced by pentylenetetrasol (n=14) 2-Pentylenetetrasol convulsion in with bilateral ligation of arteria carotis communis (n=10) 3-Group in which arteria carotis communis was opened immediately after administration of pentylenetetrasole (reperfusion group )(n=12) 4-AP group in which blood pressure was raised by use of pentylenetetrasole and immediately reduced by administration of GABA ( AP=maximal blood pressure-control blood pressure)(n=12) C-Acute Hypertension Groups 1-Acute adrenaline hypertension (n=17) 2- AP group in which acute adrenaline hypertension was induced following administration of nifedipine, a Ca-antogonist which caused a decrease in blood pressure (n=7) 3-Groups in which the right arteria carotis communis was clamped for 3 hours followed by reperfusion at different periods in each group and then adrenaline administration leading to caused hypertension.¦58- a-Reperfusion for a period of 5 minutes + Adrenaline hyperten sion (n=ll) b-Reperfusion for a period of 30 minutes + Adrenaline hyper tension (n=10) c-Reperfusion for a period of 180 minutes + Adrenaline hyper tension (n=10) d-Groups in which Evans-blue albumine extravasation was observed reperfusion at 5th, 30th, 180th minutes without inducing adrenaline hypertension (for each group n=10). For this purpose, breakdown in blood-brain barrier was determined both macroscopically according to Rapoport criteria and quantitatively by spectrophotometrical values in convulsions induced by pentylene- tetrasoleand during bilateral ligation of arteria carotis communis and in convulsions induced during reperfusion phase. An increase was noted in blood-brain barrier permeability in 92% of animals in which generalized epileptic seizures were produced by administration of pentylenetetrasole 80 mgr/kg. These increase in permeability where usually observed in the thalamus, hypothalamus, substantia nigra, corpus striatum and medulla oblongata. Under the same experimental conditions, the Evans-blue concentration was found to be 1.040+0.321 mgr % also in this group by spectrophoto metry examination. A+l breakdown of blood-brain barrier was observed in 7 animals belonging to the group in which bilateral ligation of arteria carotis communis was made. The breakdown regions were located usually in the cortex. Breakdown was also observed in the thalamic nuclei of 3 out of 7 animals. Spectrophotometry method revealed a decrease of 0.549+0.121 mgr % in Evans-blue concentration in this group. The difference between breakdown caused by pentylenetetrasole seizures and the breakdown produced during seizures when the arteria carotis communis was ligated was found to be significant (p^O.Ol). In brains in which the carotis clamp was romeved and seizures were induced during reperfusion, the Evans-blue concentration was found to-59- be very close to Evans-blue concentration during pentylenetetrasole convulsions. In this group Evans-blue concentration rose up to 0.967+0.321 mgr %. Breakdown areas of the blood-brain barrier were found to be extended in the cortex and especially in the cerebellum in the reperfusion group just like the group in which a bilateral ligation of arteria carotis communis was made. In order to study the effect of alone which is a component of blood pressure, in this group administration of pentylenetetrasole caused convulsions and increase in blood pressure and after in administration of 100 mgr/kg GABA blood pressure was reduced to control values. An increase in blood-brain barrier permeability was obsorved only in one of animals in which blood pressure was increased to a maximum and then immediately decreased. In the adrenaline AP group in which blood pressure was increased by administration of adrenaline followed by a reduction to control values by immediate administration of Ca-antagonist, no change was found in the blood-brain barrier permeability. In this group, Evans- blue concentration remained at 0.301+0.43 mgr %. Although blood pressure reached a high degree in this group, AP alone was not effective in the breakdown of the blood-brain barrier. According to these results, we can state that the principal mechanism responsible for breakdown of the blood-brain barrier during convulsions and acute hypertension is maximal blood pressure and its duration at this maximal level. No significant difference was noted between the right and the left hemispheres in the effect of acute adrenaline hypertension on the blood-brain barrier. A comparison of the amounts of Evans-blue in the right and the left hemispheres and the cerebellum with the control value yielded a signi ficant difference (p
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