Prostaglandin biosynthesis does not participate in hypercapnia-induced cerebral vasodilatation in the dog.

The participation of cerebral prostaglandin biosynthesis in hypercapnia-induced cerebral vasodilation was assessed in pentobarbital-anesthetized dogs using the radioactive microsphere technique. In five dogs, administration of 5% CO2 increased pCO2 from 31.0 +/- 0.8 to 53.4 +/- 2.4 mm Hg (P less than .001) and decreased total cerebral vascular resistance from 11.2 +/- 3.0 to 2.6 +/- 0.6 mm Hg . min . 100 g . ml-1 (P less than .001). The observed increases in pCO2 and the decreases in cerebral vascular resistance during 5% CO2 inhalation were unchanged 1 hr after administration of an i.v. bolus of 0.1 M Na2CO3 (vehicle). In another group of five dogs, 5% CO2 increased pCO2 from 30.4 +/- 0.58 to 55.2 +/- 4.2 mm Hg (P less than .01) and decreased total cerebral vascular resistance from 5.7 +/- 0.6 to 1.8 +/- 0.4 mm Hg . min . 100g . ml-1 (P less than .001). In these dogs, the CO2-induced decrease in cerebral vascular resistance 1 hr after a bolus dose of indomethacin (10 mg/kg i.v.) dissolved in 0.1 M Na2CO3 was also unchanged. In both groups of dogs the patterns described for total cerebral vascular resistance were also observed in the cerebrum, cerebellum and brainstem. The dose of indomethacin used in this study abolished the vasodepressor responses to i.v. arachidonic acid and suppressed the total brain secretion rate of immunoreactive 6-keto-prostaglandin F1 alpha. Furthermore, the administration of 5% CO2 did not increase the total brain secretion rate of immunoreactive 6-keto-prostaglandin F1 alpha. We conclude that cerebral prostaglandin biosynthesis does not mediate or modulate hypercapnia-induced cerebral vasodilation in the dog.