The effect of normothermic and hypothermic hypoxia-ischemia on brain hypoxanthine phosphoribosyl transferase activity.

Abstract:

OBJECTIVES:Cerebral hypoxia-ischemia leads to the depletion of ATP. Hypoxanthine, a degradation product of ATP, can be salvaged by hypoxanthine phosphoribosyl transferase (HPRT) and used to reform high-energy purines. Hypothermia conserves ATP in hypoxia-ischemia, possibly by preserving HPRT activity. We hypothesized that cerebral hypoxia-ischemia would decrease the activity of this enzyme, and that this reduction would be attenuated by moderate hypothermia. METHODS:Three groups of rabbits were evaluated. Normothermic rabbits were exposed to 8 minutes of hypoxia, 8 minutes of cerebral ischemia, and 30 minutes or 4 hours of cerebral reperfusion. Hypothermic rabbits were cooled to a brain temperature of 33-34 degrees C throughout identical injury and reperfusion periods. Control rabbits underwent the same preparation, without hypothermia or injury. HPRT activity in the cortex, hippocampus, thalamus, caudate, and cerebellum was measured spectrophotometrically. RESULTS:There were no significant differences (p>0.05) in enzymatic activity when comparing the three groups of animals, regardless of reperfusion time or brain temperature. Within the control group, some regional differences in enzyme activity were noted. DISCUSSION:The results indicate that brain HPRT activity is unaffected by hypoxia-ischemia, even after 4 hours of reperfusion and regardless of brain temperature. This study supports the importance of this enzyme in the conservation of brain purines after neurologic injury.

journal_name

Neurol Res

journal_title

Neurological research

authors

Cherin T,Catbagan M,Treiman S,Mink R

doi

10.1179/016164105X49229

subject

Has Abstract

pub_date

2006-12-01 00:00:00

pages

831-6

issue

8

eissn

0161-6412

issn

1743-1328

journal_volume

28

pub_type

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