Brain energy metabolism in angiotensin-induced acute hypertension in rats.
In order to study if rapid elevation of blood pressure is associated with cerebral ischemia, anesthetized (70% N2O) and artificially ventilated rats were subjected to angiotensin-induced hypertension. After a 5 min hypertensive period, cerebral cortex tissue was frozen in situ for subsequent measurements of labile glycolytic metabolites, ammonia, and organic phosphates. The degree of hypertension induced, which gave evidence of blood-brain barrier damage in 7 of 8 rats, did not affect the tissue concentrations of labile metabolites. It is concluded that ischemia does not contribute to the barrier damage, nor is it likely to be the cause of the clinical symptoms that may occur in conscious rats in the same experimental model.
D000208:Acute Disease; D000641:Ammonia / Q000378:metabolism; D000804:Angiotensin II; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000378:metabolism; D008297:Male; D009943:Organophosphorus Compounds / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D009943:Organophosphorus Compounds; D000804:Angiotensin II; D000641:Ammonia; D006003:Glycogen; D005947:Glucose