Lactic acidosis and recovery of neuronal function following cerebral hypoxia in vitro.
The rat hippocampal slice preparation was used to study the combined effects of hypoxia and lactic acidosis on neuronal function. Control slices were exposed to a standard hypoxic insult while being perfused with normal artificial cerebrospinal fluid (ACSF). Experimental slices were perfused with ACSF containing 1.0, 2.0, 10.0 or 20.0 mM lactic acid, 30 min before and during the same standard hypoxic insult. Following at 30-min recovery period the ability of these slices to respond to orthodromic stimulation by displaying a population spike (synaptic function) was tested. No significant decreases in the recovery rate of synaptic function were found between control and experimental groups, excluding the combination of 20 mM lactic acid and 10 min hypoxia, where such a decrease was found. The combination of 10 mM lactic acid and 12 min hypoxia brought about an increase in the recovery rate of synaptic function. Thus, the adverse effects attributed to lactic acid in vivo were not seen in the present in vitro study. Neuronal tissue appears to be able to handle excess lactic acid by yet, unknown mechanism (high intracellular buffer capacity?). The suggested in vivo damage due to lactic acidosis could originate in the cerebrovascular system. On the other hand, the possibility that lactic acidosis is harmless under hypoxic conditions should also be considered.
Schurr
A
A
Department of Anesthesiology, University of Louisville School of Medicine, KY 40292.
Dong
W Q
WQ
Reid
K H
KH
West
C A
CA
Rigor
B M
BM
D000140:Acidosis, Lactic / Q000139:chemically induced / Q000503:physiopathology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D007773:Lactates / Q000494:pharmacology; D019344:Lactic Acid; D008297:Male; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains
D007773:Lactates; D019344:Lactic Acid