Role of prostacyclin in the response of cerebral blood flow to CO2.
The prostacyclin (PGI2) formation in cerebral vessels, as reflected by the difference in concentration of internal carotid arterial and internal jugular venous radioimmunoassayed 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), was determined under normocapnic and hypercapnic conditions in 5 patients with mild cerebral thrombotic infarction. There was no evidence that endogenous PGI formation in cerebral vessels was stimulated at mild hypercapnia, while an increase of cerebral blood flow (CBF) induced by hypercapnia was observed. These results suggest that endogenous PGI2 may not be a mediator for the response of CBF to CO2.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000368:Aged; D001921:Brain / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood*; D002560:Cerebrovascular Circulation; D011464:Epoprostenol / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D011453:Prostaglandins / Q000097:blood*
D011453:Prostaglandins; D002245:Carbon Dioxide; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D010100:Oxygen