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Tavşanlarda deneysel üçlü subaraknoid kanama modelinde potasyum kanal aktivatörü Lemakalim'in vazospazm üzerine etkisinin değerlendirilmesi

Effects of potassium channel activator, Lemakalim, on vasospasm with triple subarachnoid hemorrhage model on rabbits

  1. Tez No: 90409
  2. Yazar: HAKAN TUNA
  3. Danışmanlar: PROF. DR. CUMHUR DİNÇER
  4. Tez Türü: Tıpta Uzmanlık
  5. Konular: Nöroşirürji, Neurosurgery
  6. Anahtar Kelimeler: Lemakalin, Potasyum kanalları, Subaraknoid kanama, Vazospazm-intrakraniyal, İskemik atak-geçici, Lemakalin, Potassium channels, Subarachnoid hemorrhage, Vasospasm-intracranial, Ischemic attack-transient
  7. Yıl: 2000
  8. Dil: Türkçe
  9. Üniversite: Ankara Üniversitesi
  10. Enstitü: Tıp Fakültesi
  11. Ana Bilim Dalı: Nöroşirürji Ana Bilim Dalı
  12. Bilim Dalı: Belirtilmemiş.
  13. Sayfa Sayısı: Belirtilmemiş.

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Özet (Çeviri)

ABSTRACT Cerebral vasospasm is a primary complication after aneurysmal subarachnoid hemorrhage (SAH). Recent evidence indicates that the activation of potassium (K+) channels may be of benefit in relieving spastic constriction. The present study examined the effects of systemic administration of a K+ channel activator, lemakalim, on cerebral vasospasm after experimental SAH. Experimental SAH was performed in rabbits by injecting autologous blood into the cisterna magna three times. Intravenous injections of lemakalim or vehicle were administered at 24'th, 36'th and 48'th hours after induction of first SAH. Second and third SAH's were performed at 24'th and 48'th hours after induction of first SAH. Digital subtraction angiography were performed on pre-SAH as a baseline, five minutes and 72 hours after first SAH to demonstrate vasospasm due to SAH and response to the treatment. Animals were killed by perfusion-fixation 72 hours after SAH. Basilar arteries were removed and sectioned, and the luminal endothelial structures were studied with electron microscope. Experimental SAH induced cerebral vasospasm in untreated and vehicle-treated animals. Lemakalim attenuated cerebral vasospasm in every dose that is given. This effect achieved statistical significance at doses of 0.03, 0.1 and 0.3 mg/kg. These results support the concept that targeting vascular K+ channels can be of benefit in preventing the development of cerebral vasospasm. The findings also indicate that lemakalim represents a potential therapeutic agent for the treatment of cerebrovascular pathophysiology after SAH.

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