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Oxypurines in cerebrospinal fluid as indices of disturbed brain metabolism. A clinical study of ischemic brain diseases.
Author(s) -
Roger Hällgren,
Frank Niklasson,
Andreas Terént,
Axel Åkerblom,
E. Widerlöv
Publication year - 1983
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.14.3.382
Subject(s) - medicine , hypoxanthine , xanthine , hypoxia (environmental) , cerebrospinal fluid , uric acid , endocrinology , ischemia , cerebral edema , brain damage , cerebral infarction , xanthine oxidase , albumin , cardiology , pathology , biochemistry , oxygen , enzyme , biology , chemistry , organic chemistry
Using a HPLC method the concentrations of oxypurines were simultaneously measured in CSF of patients with acute cerebrovascular lesions (CVL) and global cerebral ischemia (GCI) in an attempt to study disturbed brain metabolism during cerebral oxygen deprivation. In cerebral infarction both hypoxanthine and xanthine gradually increased from normal levels at admission to pathologically increased on the fourth day from onset of symptoms. There was no correlation between these substances and the clinical score but the maximum CSF-hypoxanthine concentration was significantly correlated to the maximum lesion volume determined by computerized tomography. In GCI the hypoxanthine-xanthine concentrations were considerably increased less than 20 hours from onset of unconsciousness but the initial levels did not predict the final outcome. These findings suggest that the end products of nucleotide degradation accumulate rapidly in acute cerebral hypoxia but more gradually in CVL probably due to growing local edema with subsequent local hypoxia. In controls and patients with CVL the CSF-urate concentrations were positively correlated to those of CSF-albumin. However, in CVL the increase of urate was relatively much more pronounced than the increase of albumin indicating that urate is a sensitive marker of dysfunction of blood-brain barrier.

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