Pretražite po imenu i prezimenu autora, mentora, urednika, prevoditelja

Napredna pretraga

Pregled bibliografske jedinice broj: 47894

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


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)
Pariz, Francuska, 1998. str. 275-276 (poster, međunarodna recenzija, sažetak, znanstveni)


CROSBI ID: 47894 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

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

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

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Abstracts of the XIth Congress of the European College of Neuropsychopharmacology ; u: European Neuropsychopharmacology. Supplement 8 (1998) (S2) / - , 1998, 275-276

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

Mjesto i datum
Pariz, Francuska, 31.10.-04.11.1998

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Sažetak
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.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti



POVEZANOST RADA


Projekti:
062028

Ustanove:
Medicinski fakultet, Rijeka


Citiraj ovu publikaciju

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)
Pariz, Francuska, 1998. str. 275-276 (poster, međunarodna recenzija, sažetak, znanstveni)
Mršić, J., Maysinger, D., Župan, G. & Simonić, A. (1998) Effects of calcium channel blockers, MK-801 and nimodipine on the Na, K-ATPase activity in rats exposed to hypoxia and cerebral ischemia. U: Abstracts of the XIth Congress of the European College of Neuropsychopharmacology ; u: European Neuropsychopharmacology. Supplement 8 (1998) (S2).
@article{article, year = {1998}, pages = {275-276}, keywords = {}, title = {Effects of calcium channel blockers, MK-801 and nimodipine on the Na, K-ATPase activity in rats exposed to hypoxia and cerebral ischemia}, keyword = {}, publisherplace = {Pariz, Francuska} }
@article{article, year = {1998}, pages = {275-276}, keywords = {}, title = {Effects of calcium channel blockers, MK-801 and nimodipine on the Na, K-ATPase activity in rats exposed to hypoxia and cerebral ischemia}, keyword = {}, publisherplace = {Pariz, Francuska} }




Contrast
Increase Font
Decrease Font
Dyslexic Font