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

Al-Olama M, Lange S, Lönnroth I, Gatzinsky K, Jennische E - Acta Neurochir (Wien) (2014)

Bottom Line: The continuous ICP registrations were achieved by means of telemetry.Intranasal administration of AF-16 suppressed the increased ICP to normal values within 30 min.The ability of AF-16 to suppress an increased ICP was manifested.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, P.O.B. 440, 405 30, Göteborg, Sweden.

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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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Related in: MedlinePlus

Recordings of ICP 24 h after a cryogenic injury. a Before anaesthesia. b Transient increase in ICP during induction of anaesthesia. c Return to the pre-anaesthetic level after a couple of minutes. d Reduced ICP 30 min after AF-16 administration
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Fig5: Recordings of ICP 24 h after a cryogenic injury. a Before anaesthesia. b Transient increase in ICP during induction of anaesthesia. c Return to the pre-anaesthetic level after a couple of minutes. d Reduced ICP 30 min after AF-16 administration

Mentions: The induction of anaesthesia caused a transient increase in ICP (Fig. 5), but after 3–5 min ICP returned to pre-treatment levels, after which AF-16 or the vehicle (PBS) was administered intranasally. Table 2 shows the mean decrease in ICP in percent after intranasal administration of AF-16 or PBS, respectively. The decrease in ICP is calculated as the difference between the initial, pre-treatment levels and the mean of ICP recordings during the first 20-min period after the animals had fully recovered from anaesthesia. ICP decreased from initial, pre-treatment level of 10.01 ± 1.99 mmHg to 7.93 ± 1.31 mmHg in rats (n = 10) treated intranasally with PBS. In rats (n = 10) given AF-16 intranasally the ICP decreased from 10.06 ± 1.84 mmHg to 6.09 ± 1.03 mmHg. The ICP reduction was significantly larger in the AF-16-treated animals than in the PBS-treated animals (p < 0.002). A typical course with reduction in ICP after intranasal administration of AF-16 in an animal subjected to a cryogenic brain injury is shown in Fig. 5.Fig. 5


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

Al-Olama M, Lange S, Lönnroth I, Gatzinsky K, Jennische E - Acta Neurochir (Wien) (2014)

Recordings of ICP 24 h after a cryogenic injury. a Before anaesthesia. b Transient increase in ICP during induction of anaesthesia. c Return to the pre-anaesthetic level after a couple of minutes. d Reduced ICP 30 min after AF-16 administration
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4281356&req=5

Fig5: Recordings of ICP 24 h after a cryogenic injury. a Before anaesthesia. b Transient increase in ICP during induction of anaesthesia. c Return to the pre-anaesthetic level after a couple of minutes. d Reduced ICP 30 min after AF-16 administration
Mentions: The induction of anaesthesia caused a transient increase in ICP (Fig. 5), but after 3–5 min ICP returned to pre-treatment levels, after which AF-16 or the vehicle (PBS) was administered intranasally. Table 2 shows the mean decrease in ICP in percent after intranasal administration of AF-16 or PBS, respectively. The decrease in ICP is calculated as the difference between the initial, pre-treatment levels and the mean of ICP recordings during the first 20-min period after the animals had fully recovered from anaesthesia. ICP decreased from initial, pre-treatment level of 10.01 ± 1.99 mmHg to 7.93 ± 1.31 mmHg in rats (n = 10) treated intranasally with PBS. In rats (n = 10) given AF-16 intranasally the ICP decreased from 10.06 ± 1.84 mmHg to 6.09 ± 1.03 mmHg. The ICP reduction was significantly larger in the AF-16-treated animals than in the PBS-treated animals (p < 0.002). A typical course with reduction in ICP after intranasal administration of AF-16 in an animal subjected to a cryogenic brain injury is shown in Fig. 5.Fig. 5

Bottom Line: The continuous ICP registrations were achieved by means of telemetry.Intranasal administration of AF-16 suppressed the increased ICP to normal values within 30 min.The ability of AF-16 to suppress an increased ICP was manifested.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, P.O.B. 440, 405 30, Göteborg, Sweden.

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Show MeSH
Related in: MedlinePlus