Does thromboxane A2 synthase inhibitor UK-38485 prevent the vasoconstrictor effects of endothelin-1 on rabbit basilar artery?


Baykaner M., Keskil I., Sencer H., Ilgit E. T. , Ataoglu O., Ceviker N., ...Daha Fazla

Acta Neurochirurgica, cilt.141, sa.3, ss.279-285, 1999 (SCI Expanded İndekslerine Giren Dergi) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 141 Konu: 3
  • Basım Tarihi: 1999
  • Doi Numarası: 10.1007/s007010050299
  • Dergi Adı: Acta Neurochirurgica
  • Sayfa Sayıları: ss.279-285

Özet

Prevention of the production of thromboxane A2 - a potent vasoconstrictor and aggregating metabolite of arachidonic acid - or infusion of the stable analogues of prostacyclin - which is another cyclooxygenase metabolite of arachidonic acid - has been shown to be beneficial in cerebral vasoconstriction. Endothelin-1, a peptide derived from endothelial cells, has been shown to induce a long-lasting cerebral vasoconstriction both in vivo and in vitro. The purpose of this study was to investigate the rule of a novel thromboxane A2-synthase inhibitor UK 38485 on the acute vascular and morphological effects of Endothelin-1 applied intra-arterially on rabbit basilar arteries. The inguinal region of twenty four anaesthetized albino rabbits of both sexes were dissected and a catheter was inserted into the aorta via the femoral artery, for control angiography of the basilar artery and intra-arterial injection of ET-1 (0.25 ng total dose) and UK 38485 at a dose of 0.05 μg kg-1 min-1 for 20 min or saline. Angiographic vasoconstriction quantification and morphological investigations of both vessels and brain stem either by light microscopy or transmission electron microscopy were the techniques applied for the study. We found out that, although the systemic administration of UK 38485 resulted in a potent antagonism of the acute vasoconstriction as visualized in angiographic studies, it did not affect the morphological changes induced by Endothelin-1 on the vessel wall. The results indicated that there might have been an interaction between Endothelin-1 and the prostaglandin synthesis mechanism in acute cerebral vasoconstriction.