Nalazite se na CroRIS probnoj okolini. Ovdje evidentirani podaci neće biti pohranjeni u Informacijskom sustavu znanosti RH. Ako je ovo greška, CroRIS produkcijskoj okolini moguće je pristupi putem poveznice www.croris.hr
izvor podataka: crosbi

Effects of calcium channel blockers, MK-801 and nimodipine on the Na, K-ATPase activity in rats exposed to hypoxia and cerebral ischemia (CROSBI ID 475489)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija

Mršić, Jasenka ; Maysinger, Dušica ; Župan, Gordana ; Simonić, Ante Effects of calcium channel blockers, MK-801 and nimodipine on the Na, K-ATPase activity in rats exposed to hypoxia and cerebral ischemia // Abstracts of the XIth Congress of the European College of Neuropsychopharmacology ; u: European Neuropsychopharmacology. Supplement 8 (1998) (S2). 1998. str. 275-276

Podaci o odgovornosti

Mršić, Jasenka ; Maysinger, Dušica ; Župan, Gordana ; Simonić, Ante

engleski

Effects of calcium channel blockers, MK-801 and nimodipine on the Na, K-ATPase activity in rats exposed to hypoxia and cerebral ischemia

Background and Purpose: The pathogenesis of hypoxic/ischemic brain injury is closely related to the excessive release of glutamate (Glu). The results of recent studies strongly support the hypothesis that a crucial role in Glu neurotoxicity during hypoxia/ischemia plays sustained increase in intracellular calcium concentration (Ca2+)i, mostly through receptor operated calcium channels (NMDA receptors) and/or voltage dependent calcium channels (VDCC). Moreover, several authors have shown that increase in (Ca2+)i inhibits the activity of Na, K-ATPase, the membrane bound enzyme that plays a vital role in the functioning of all higher eukaryotic cells. Since pharmacotherapy of hypoxic/ischemic brain injury is still unefficient, our goal was to examine the efiects of MK-801, NMDA receptor antagonist and nimodipine, VDCC blocker on Na, K-ATPase activity in rats exposed to hypoxia and global cerebral ischemia. Methods: Animals: Hannover-Wistar rats, weighing 250 g. Models:Hypoxia: In hypoxia cage the oxygen concentration was gradually reduced until the level of 3.5 V% of oxygen was reached. The animals were maintained in such conditions until loosing righting refiex. Mentioned experimental procedure lasted 20-25 min. Global cerebral ischemia: vertebral arteries were occluded by electrocautery at the level of the first cervical vertebra. The day after, the common carotid arteries were exposed and a forebrain ischemia was produced by tightening the carotid artery clips for 20 min. Na, K-ATPase assay: NKA activity was determined spectrophotometrically by modification of the method described by Stefanovic et al. (1974). Procedure: Animals were exposed to a) controlled hypoxic conditions or b) global cerebral ischemia or c) pretreatment with difierent doses (0.03 ; 0. 1 ; 0.3 or 1.0 mg/kg) of MK-801 or nimodipine, 30 min before hypoxic or ischemic insult, and after difierent period of time (30 min, 4 hr, 24 hr or 72 hr), Na, K-ATPase activity was measured in hippocampus and cortex. Results: Statistically significant decrease in Na, K-ATPase activity was found after 4 hr, 24 hr and 72 hr of hypoxic insult. In ischemic conditions we found transient increase of enzymatic activity after 30 min, but profound and significant decrease after 4 hr-72 hr. Nimodipine prevented decrease in Na, K-ATPase activity in animals exposed to hypoxia in dose 1.0 mg/kg, while in ischemic conditions we did not find any significant changes in Na, K-ATPase activity between animals pretreated with nimodipine or non treated animals. Pretreatment with 1.0 mg/kg of MK-80l preserved Na, K-ATPase activity in both hypoxic and ischemic conditions. Conclusion: Decrease in Na, K-ATPase activity is evident in both hypoxic and ischemic conditions. Transient increase in enzymatic activity in ischemic conditions is probably an attempt to maintain ion and glutamate homeostasis under restricted energy and oxygen supply. Pretreatment with calcium channel blockers like nimodipine or MK801 may have utility in treatment of hypoxic/ischemic neuronal injury. Blocade of NMDA receptors by MK-801 seems to be more effective in preventing neuronal damage than VDCC blockade by nimodipine.

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

Podaci o prilogu

275-276.

1998.

nije evidentirano

objavljeno

Podaci o matičnoj publikaciji

Abstracts of the XIth Congress of the European College of Neuropsychopharmacology ; u: European Neuropsychopharmacology. Supplement 8 (1998) (S2)

Podaci o skupu

Congress of the European College of Neuropsychopharmacology (11 ; 1998)

poster

31.10.1998-04.11.1998

Pariz, Francuska

Povezanost rada

Temeljne medicinske znanosti