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Hydrogen ions kill brain at concentrations reached in ischemia.
Summary
Excessive lactic acid in the brain, especially during ischemia, can cause brain necrosis. Acidosis below pH 5.30 is critical for this neurotoxicity, leading to infarction.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Brain glucose elevation before ischemia increases lactic acid, potentially causing acidosis.
- Acidosis may be a key factor in transforming selective neuronal loss into ischemic brain infarction.
Purpose of the Study:
- To investigate the neurotoxic effects of excessive lactic acid concentrations in the brain.
- To determine the critical pH threshold for lactic acid-induced brain necrosis.
Main Methods:
- Microinjection of 150 mM sodium lactate solutions at varying pH levels into the rat parietal cortex.
- Monitoring of interstitial pH (pH0) using hydrogen ion-selective microelectrodes.
- Histological examination of brain tissue 24 hours post-injection.
Main Results:
- Brain necrosis resembling ischemic infarction occurred only when interstitial pH (pH0) dropped to 5.30 or below.
- Nonlethal injections resulted in minor needle tract injuries.
- Lethal injections showed a slower return of pH0 to baseline, indicating impaired acid-base homeostasis.
Conclusions:
- Excessive lactic acid, particularly at pH ≤ 5.30, is neurotoxic and can induce brain necrosis similar to ischemic infarction.
- Impaired brain acid-base regulation, potentially due to altered membrane transport and buffer loss, is associated with this necrosis.