Acidosis and neuroprotection in two types of acidosis model rats under isoflurane anesthesia: evaluation of blood flow, pH and amino acid levels in the cortex

• Published in: Masui. The Japanese journal of anesthesiology Vol. 47; no. 10; p. 1173
• Main Authors: Shimizu, A, Kusagaya, H, Issiki, A
• Format: Journal Article
• Language: Japanese
• Published: Japan 01.10.1998
• Subjects: Acidosis - physiopathology; Anesthesia, Inhalation; Anesthetics, Inhalation; Animals; Cerebral Cortex - blood supply; Disease Models, Animal; Glutamic Acid - metabolism; Hydrogen-Ion Concentration; Isoflurane; Male; Rats; Rats, Wistar; Regional Blood Flow
• ISSN: 0021-4892

In order to evaluate the effect of brain acidosis on neuronal functions as assessed by the in vivo studies, changes of cerebral blood flow (CBF), brain pH ([pH]o) and brain amino acid levels in the same brain region of the two different acidosis model rats were measured under isoflurane anesthesia. Three micro probes to measure CBF, [pH]o and amino acids, respectively, were implanted into the frontal cortex, and these parameters were recorded simultaneously. In the metabolic acidosis rats, the sustained decrease of [pH]o and amino acid levels, particularly Glu, were detected after the treatment with 10 min-i.v. infusion of 1 N HCl, although the significant changes of CBF did not appear because of the respiratory management. In the respiratory acidosis model, however, transient and significant increase of CBF and decrease of Glu and [pH]o were recorded after 10 min-exposure to about 30% CO2 (N2O:O2:CO2 = 2:5:3). The levels of Gly and Gln were reduced after acute exposure to hypercapnia, but these levels recovered to the control level in 20-30 min after hypercapnia exposure. In both animals, the amounts of Tau was gradually reduced after the treatment with 1 N HCl and hypercapnia, and these levels did not return to the control level when other amino acid levels had recovered. These differences of brain amino acid levels in the two different types of acidosis model rats may be related to the brain amino acid metabolic pathway. Thus, during brain acidosis induced by 1 N HCl and hypercapnia, the amount of extracellular Glu in the brain was reduced, and this reduction may contribute to the neuroprotective effects.