Navigation überspringen
Universitätsbibliothek Heidelberg
Status: Bibliographieeintrag

Verfügbarkeit
Standort: ---
Exemplare: ---
heiBIB
 Online-Ressource
Verfasst von:Sánchez-Porras, Renán [VerfasserIn]   i
 Kentar, Modar [VerfasserIn]   i
 Zerelles, Roland [VerfasserIn]   i
 Geyer, Martina [VerfasserIn]   i
 Trenado Colin, Carlos Alberto [VerfasserIn]   i
 Hartings, Jed A. [VerfasserIn]   i
 Woitzik, Johannes [VerfasserIn]   i
 Dreier, Jens P. [VerfasserIn]   i
 Santos, Edgar [VerfasserIn]   i
Titel:Eighteen-hour inhibitory effect of s-ketamine on potassium- and ischemia-induced spreading depolarizations in the gyrencephalic swine brain
Verf.angabe:Renán Sánchez-Porras, Modar Kentar, Roland Zerelles, Martina Geyer, Carlos Trenado, Jed A. Hartings, Johannes Woitzik, Jens P. Dreier, Edgar Santos
E-Jahr:2022
Jahr:5 July 2022
Umfang:14 S.
Fussnoten:Gesehen am 10.11.2022
Titel Quelle:Enthalten in: Neuropharmacology
Ort Quelle:Amsterdam [u.a.] : Elsevier Science, 1970
Jahr Quelle:2022
Band/Heft Quelle:216(2022), Artikel-ID 109176, Seite 1-14
ISSN Quelle:1873-7064
Abstract:Spreading depolarizations (SDs) are characterized by near-complete breakdown of the transmembrane ion gradients, cytotoxic edema, and glutamate release. SDs are associated with poor neurological outcomes in cerebrovascular diseases and brain trauma. Ketamine, a N-methyl-d-aspartate receptor antagonist, has shown to inhibit SDs in animal models and in humans. However, little is known about its SD-inhibitory effect during long-term administration. Lissencephalic animal models have shown that ketamine loses its SD-blocking effect after some minutes to hours. Physio-anatomical differences between lissencephalic and the more evolved gyrencephalic animals may affect their SDs-blocking effect. Therefore, information from the last may have more translational potential. Therefore, the aim of this study was to investigate the 18 h-effect of s-ketamine as a basis for its possible long-term clinical use for neuroprotection. For this purpose, two gyrencephalic swine brain models were used. In one, SDs were elicited through topical application of KCl; in the other model, SDs were spontaneously induced after occlusion of the middle cerebral artery. S-ketamine was administered at therapeutic human doses, 2, 4 and 5 mg/kg BW/h for up to 18 h. Our findings indicate that s-ketamine significantly reduces SD incidence and expansion without clear evidence of loss of its efficacy. Pharmacological susceptibility of SDs to s-ketamine in both the ischemic gyrencephalic brain and well-perfused brain was observed. SDs were most potently inhibited by s-ketamine doses that are above the clinically recommended (4 mg/kg BW/h and 5 mg/kg BW/h). Nonetheless, such doses are given by neurointensivists in individual cases. Our results give momentum to further investigate the feasibility of a multicenter, neuromonitoring-guided, proof-of-concept clinical trial.
DOI:doi:10.1016/j.neuropharm.2022.109176
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1016/j.neuropharm.2022.109176
 Volltext: https://www.sciencedirect.com/science/article/pii/S0028390822002350
 DOI: https://doi.org/10.1016/j.neuropharm.2022.109176
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Electrocorticography
 Gyrencephalic brain
 Ketamine
 Neuromonitoring
 Spreading depolarization
 Stroke
K10plus-PPN:1821596137
Verknüpfungen:→ Zeitschrift

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/68984070   QR-Code
zum Seitenanfang