The influence of fentanyl upon cerebral high-energy metabolites, lactate, and glucose during severe hypoxia in the rat

• Published in: Anesthesiology (Philadelphia) 1988-10, Vol.69 (4), p.566-570
• Main Authors: MEHDI KEYKHAH, M, SMITH, D. S, O'NEIL, J. J, HARP, J. R
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - metabolism; Anesthetics. Neuromuscular blocking agents; Animals; Biological and medical sciences; Brain - metabolism; Electroencephalography; Energy Metabolism; Fentanyl - pharmacology; Glucose - metabolism; Hypothermia, Induced; Hypoxia - metabolism; Hypoxia - physiopathology; Lactates - metabolism; Lactic Acid; Male; Medical sciences; Neuropharmacology; Oxygen Consumption - drug effects; Pentobarbital - pharmacology; Pharmacology. Drug treatments; Phosphocreatine - metabolism; Rats; Space life sciences
• ISSN: 0003-3022; 1528-1175
• DOI: 10.1097/00000542-198810000-00017

The effects of intravenous administration of high-dose fentanyl (100 micrograms.kg-1, loading dose followed by an infusion of 200 micrograms.kg-1.h-1) were compared with those of a barbiturate (pentobarbital sodium 25 mg.kg-1, intraperitoneal) or hypothermia (rectal temperature 32 degrees C) on changes in cerebral cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine (PCr), lactate, and glucose in severely hypoxemic rats (PaO2 13-23 mmHg for 20 min) with unilateral (left side) carotid ligation (10-12 animals in each group). Ligation of the carotid artery alone produced no change in brain high-energy metabolites, lactate, or glucose. The control values on the ligated side (nitrous oxide, 70%, + normoxia group) for cortical ATP, PCr, lactate, and glucose were 2.86 +/- 0.09 (mumol.g-1 wet weight, mean +/- 1 SE), 3.83 +/- 0.11, 1.68 +/- 0.21, and 3.29 +/- 0.47, respectively. Hypoxia (nitrous oxide, 70%, + hypoxia group) produced a significant (P less than 0.05) decrease in ATP (1.83 +/- 0.37) and PCr (1.93 +/- 0.48) and an increase in lactate (15.8 +/- 1.77) compared with the normoxic group, whereas brain glucose was not significantly changed (1.97 +/- 0.65). Fentanyl (fentanyl + hypoxia group) did not prevent the deleterious effects of hypoxia on cortical high energy metabolites (ATP, 2.0 +/- 0.27; PCr, 2.24 +/- 0.3) or lactate (19.33 +/- 3.16); however, fentanyl caused no alteration in high-energy cerebral metabolite concentrations in normoxic rats, nor did fentanyl produce a significant difference in brain tissue glucose or lactate.