Monitoring arterio-venous differences of glucose and lactate in the anesthetized rat with or without brain damage with ultrafiltration and biosensor technology

Continuous monitoring of arterio‐venous glucose and lactate differences may serve as a diagnostic tool to assess normal brain function and brain pathology. We describe a method and some results obtained with arterio‐venous measurements of glucose and lactate in the blood of the halothane‐anesthetize...

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Bibliographic Details
Published in:Journal of neuroscience research 2001-12, Vol.66 (5), p.795-802
Main Authors: Leegsma-Vogt, Gea, Venema, Kor, Postema, Folkert, Korf, Jakob
Format: Article
Language:English
Subjects:
Anesthetics - pharmacology
Animals
Arteries - metabolism
arterio-venous differences
Biosensing Techniques - instrumentation
Biosensing Techniques - methods
Blood Glucose - physiology
brain
Brain - metabolism
Brain - physiopathology
Brain Injuries - metabolism
Cerebrovascular Circulation - physiology
Energy Metabolism - physiology
glucose
Hemofiltration - instrumentation
Hemofiltration - methods
lactate
Lactic Acid - blood
Male
Monitoring, Physiologic - instrumentation
Monitoring, Physiologic - methods
Rats
Rats, Wistar
ultrafiltration
Veins - metabolism
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Summary:Continuous monitoring of arterio‐venous glucose and lactate differences may serve as a diagnostic tool to assess normal brain function and brain pathology. We describe a method and some results obtained with arterio‐venous measurements of glucose and lactate in the blood of the halothane‐anesthetized rat and after brain injury. The method is based on low flow rate ultrafiltration for continuous collection of blood filtrate combined with flow injection analysis and biosensors for the detection of glucose and lactate. We measured the glucose and lactate concentration every minute in the jugular vein and the aorta at control conditions and during and after inflation of an embolectomy‐balloon for 2 min. Net cerebral lactate efflux and glucose uptake was seen under control conditions and at low blood lactate levels. During brain injury both lactate release and glucose uptake were reduced and there was a net lactate influx at high arterial lactate levels. These results indicate that the flux of lactate in and out of the brain is not only dependent on the lactate concentration in the brain, but on blood levels as well, possibly because of bi‐directional flux through the monocarboxylate transporter type 1. © 2001 Wiley‐Liss, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/jnr.10046