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Uptake of the antisecretory factor peptide AF-16 in rat blood and cerebrospinal fluid and effects on elevated intracranial pressure

Journal article
Authors Mohamed Al-Olama
Stefan Lange
Ivar Lönnroth
Kliment Gatzinsky
Eva Jennische
Published in Acta Neurochirurgica
Volume 157
Issue 1
Pages 129-137
ISSN 0001-6268
Publication year 2015
Published at Institute of Biomedicine
Pages 129-137
Language en
Links dx.doi.org/10.1007/s00701-014-2221-...
Keywords AF-16 uptake, Intranasal administration, Brain oedema, Intracranial pressure, Telemetry, Continuous, CENTRAL-NERVOUS-SYSTEM, INTRACEREBRAL HEMORRHAGE, INTRANASAL DELIVERY, PROTEIN, MECHANISMS, EXPRESSION, COLITIS, DEATH, Clinical Neurology, Surgery
Subject categories Neurosciences

Abstract

AF-16 is a 16-amino-acid-long peptide derived from the amino-terminal part of the endogenous protein, antisecretory factor (AF). AF-16 in vivo has been shown to regulate dysfunctions in the water and ion transport system under various pathological conditions and also to counteract experimentally increased tissue pressure. Rats were subjected to a cryogenic brain injury in order to increase the intracranial pressure (ICP). The distribution of AF-16 in blood and CSF after intravenous or intranasal administration was determined in injured and control rats. ICP was monitored in freely moving, awake rats, by means of an epidural pressure transducer catheter connected to a wireless device placed subcutaneously on the skull. The continuous ICP registrations were achieved by means of telemetry. Intranasal administration of AF-16 resulted in a significantly higher CSF concentrations of AF-16 in injured than in control rats, 1.3 versus 0.6 ng/ml, whereas no difference between injured and control rats was seen when AF-16 was given intravenously. Rats subjected to cryogenic brain injury developed gradually increasing ICP levels. Intranasal administration of AF-16 suppressed the increased ICP to normal values within 30 min. Optimal AF-16 concentrations in CSF are achieved after intranasal administration in rats subjected to a cryogenic brain injury. The ability of AF-16 to suppress an increased ICP was manifested.

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