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Changes in extracellular acid-base homeostasis in cerebral ischemia
D L Taylor1, T P Obrenovitch, L Symon
1Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom.
Neurochemical Research
|September 1, 1996
Summary
During ischemia, cellular acid-base regulation mechanisms activate but fail upon anoxic depolarization. Lactate transport is key to cell survival during these events.
Area of Science:
- Biochemistry
- Cell Physiology
- Neuroscience
Background:
- Ischemia triggers significant changes in cellular acid-base balance.
- Anoxic depolarization is a critical event during ischemic conditions.
- Organic acid transport systems play a role in cellular homeostasis.
Purpose of the Study:
- To investigate extracellular carbonate (CO32-) and lactate changes during ischemia.
- To understand the impact of anoxic depolarization on these changes.
- To determine how probenecid, an inhibitor of organic acid transport, affects these processes.
Main Methods:
- Monitoring extracellular CO32- and lactate concentrations during induced ischemia.
- Assessing the effects of probenecid on ion transport.
- Analyzing cellular membrane permeability changes in relation to anoxic depolarization.
Main Results:
- Transmembrane mechanisms for intracellular acid-base regulation (e.g., Na+/H+ exchange, lactate/H+ cotransport) are highly active during ischemia.
- Anoxic depolarization leads to increased cell membrane permeability, abolishing the effectiveness of these regulatory mechanisms.
- Lactate efflux during ischemia and reuptake during reperfusion are primarily mediated by a specific transporter.
Conclusions:
- Cellular acid-base homeostasis is maintained until anoxic depolarization occurs.
- Anoxic depolarization is a pivotal event that compromises cellular survival during ischemia.
- Inhibition of organic acid transport affects lactate dynamics during ischemia and reperfusion.
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