Endothelin-1 contributes to normocapnic hyperoxic pial artery vasoconstriction.
The present study was designed to determine if hyperoxia elicits pial artery vasoconstriction and to characterize the contribution of endothelin-1 (ET-1) to that vascular response in newborn pigs equipped with a closed cranial window. Hyperoxic conditions were established by ventilating the piglets with 100% O(2) during normocapnia and concomitantly topically applying artificial CSF that had been bubbled with 100% O(2). Hyperoxia elevated CSF ET-1 from 23+/-1 to 45+/-4 pg/ml. Hyperoxia also elicited pial artery vasoconstriction that was attenuated by BQ123 (10(-6) M), an ET-1 antagonist (-15+/-1 vs. -5+/-1%). These data indicate that ET-1 contributes to hyperoxic pial artery vasoconstriction.
Armstead
W M
WM
Departments of Anesthesia and Pharmacology, University of Pennsylvania and The Children's Hospital of Philadelphia, 34th and Civic Center Blvd., Philadelphia, PA 19104, USA.
D000818:Animals; D001160:Arterioles / Q000033:anatomy & histology / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000378:metabolism*; D002536:Cerebral Arteries / Q000187:drug effects / Q000502:physiology*; D019332:Endothelin-1 / Q000378:metabolism / Q000502:physiology*; D005260:Female; D018496:Hyperoxia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D019332:Endothelin-1; D002245:Carbon Dioxide