Abstract
Acute hyperammonemia causes glutamine and water accumulation in astrocytes and loss of the cerebral blood flow response selectively to CO2. We tested whether extraparenchymal pial arterioles not subjected directly to mechanical compression by swollen astrocyte processes also lose hypercapnic reactivity and whether any such loss can be attenuated by inhibiting glutamine synthesis during hyperammonemia. Pentobarbital-anesthetized rats were pretreated intravenously with either saline vehicle, methionine sulfoximine (0.83 mmol/kg), which inhibits glutamine synthetase and potentially gamma-glutamylcysteine synthetase, or buthionine sulfoximine (4 mmol/kg), which inhibits gamma-glutamylcysteine synthetase. Three hours after pretreatment, cohorts received an intravenous infusion of either sodium or ammonium acetate for 6 hours. Pial arteriolar diameter was measured with radiolabeled microspheres during normocapnia and 10 minutes of hypercapnia. With sodium acetate infusion, pial arteriolar diameter increased during hypercapnia in groups pretreated with vehicle (23+/-3% [mean+/-SE]; n=6), methionine sulfoximine (37+/-11%; n=5), and buthionine sulfoximine (32+/-3%; n=5). With ammonium acetate infusion, pial arteriolar diameter increased...Continue Reading
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