Changes in Glutathione Peroxidase and Lipid Peroxides in Cerebrospinal Fluid and Serum after Subarachnoid Hemorrhage

—With Special Reference to the Occurrence of Cerebral Vasospasm—

Abstract

To clarify the pathogenesis of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH), the authors studied changes in lipid peroxides (measured as thiobarbituric acid reactive substances, TRS) and their scavenging enzyme, glutathione peroxidase (GPx), in the cerebrospinal fluid (CSF) and the serum of SAH patients and normal subjects. The CSF of the normal subjects was almost devoid of both TRS and GPx. A sudden increase in GPx activity in the CSF of SAH patients appeared to be due to the efflux of serum GPx to the subarachnoid space. GPx in the CSF decreased within 2-4 days after SAH, and in some cases the TRS content then became elevated and delayed vasospasm ensued. Following SAH, serum TRS increased, reaching a plateau 4-5 days after onset. GPx also increased 1 or 2 days later. The increase in serum TRS appeared to be a consequence of blood clotting within the subarachnoid space and may have stimulated GPx activity. The findings suggest that lipid peroxides present in the CSF and the serum of SAH patients may be responsible for development of delayed vasospasm and that serum GPx might play an important role in controlling it.