[Xanthine oxidase of the cerebrospinal fluid in patients with craniocerebral trauma]. / Ksantinoksidaza spinnomozgovoi zhidkosti u bol'nykh s cherepno-mozgovoi travmoi.

The authors studied the activity of xanthine oxidase (XO) and xanthine dehydrogenase (XDG) in the cerebrospinal fluid (CSF) of patients with craniocerebral trauma (CCT). XO and XDG activity in CSF appeared in moderate and severe CCT. XO in CSF was predominantly of cerebral origin. The possible role of XO in activation of lipid peroxidation in CCT is discussed. It is suggested that determination of XO and XDG activity in CSF should be used for evaluating the severity of the trauma.

Production of uric acid in cerebrospinal fluid after subarachnoid hemorrhage in dogs: investigation of the possible role of xanthine oxidase in chronic vasospasm.

Based on accumulating evidence of the role of xanthine oxidase (XO) in generating oxygen free radicals and causing tissue damage during ischemia, we examined the possible role of XO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). After inducing SAH in dogs by two autologous blood injections 2 days apart, chronic vasospasm of the basilar artery was reliably produced. There was a 3.5-fold elevation in uric acid (UA), the product of XO, in the cerebrospinal fluid (CSF) of these animals. Parenteral administration of allopurinol (i.v., 25 mg/kg, every 6 hours), a specific blocker of XO, successfully abolished the elevation in CSF uric acid levels due to SAH. However, angiographic vasospasm measured on Day 7, morphological changes observed by electron microscope, and elevated CSF prostaglandin levels were not altered by the treatment. It can be concluded that the observed activation of the enzyme XO, which is a well-known source of oxygen free radicals in ischemia in various organs, is not playing a major role in the pathogenesis of chronic cerebral vasospasm in this animal.