Failure of brain cytochrome alpha , alpha 3 redox recovery after hypoxic hypotension as determined by in vivo reflectance spectrophotometry.
Rats were subjected to a 30 minute period of combined hypoxia (F1o2 = .08) and hemorrhagic hypotension (MAP = 30 mm Hg), then resuscitated by restoration of F1o2 = .30 and reinfusion of shed blood and saline. Intracranial blood volume, hemoglobin saturation, and the cytochrome alpha, alpha 2 redox state were monitored through the intact skull during hypoxic hypotension and after resuscitation utilizing reflectance spectrophotometry. Although resuscitation returned arterial blood pressure, arterial pO2, and hemoglobin saturation toward normal, a sustained, significant (p less than .005) reduction in cytochrome alpha , alpha 2 remained. A parallel series of rats was subjected to identical hypoxic hypotension. At designated intervals the animals were sacrificed to determine brain ATP, ADP, and inorganic phosphate (P1). The data are discussed in terms of relationships between high energy phosphate metabolism and recorded changes in cerebral cytochrome alpha , alpha 2 redox state.
D000137:Acid-Base Imbalance / Q000209:etiology; D000818:Animals; D001921:Brain / Q000201:enzymology*; D003576:Electron Transport Complex IV / Q000378:metabolism*; D006454:Hemoglobins / Q000378:metabolism; D007022:Hypotension / Q000201:enzymology* / Q000209:etiology; D000860:Hypoxia / Q000150:complications / Q000201:enzymology*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains; D013053:Spectrophotometry / Q000379:methods
D006454:Hemoglobins; D007773:Lactates; D019344:Lactic Acid; D003576:Electron Transport Complex IV