The influence of MK-801 on the hippocampal free arachidonic acid level and Na+,K+-ATPase activity in global cerebral ischemia-exposed rats

2002 ◽  
Vol 26 (7-8) ◽  
pp. 1319-1326 ◽  
Author(s):  
Jasenka Mršić-Pelčić ◽  
Gordana Župan ◽  
Dusica Maysinger ◽  
Goran Pelčić ◽  
Dinko Vitezić ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Cerebral Ischemia ◽  
Atpase Activity ◽  
Acid Level ◽  
Global Cerebral Ischemia ◽  
Arachidonic Acid Level ◽  
Mk 801 ◽  
Free Arachidonic Acid

Validation of the effects of progesterone and MK-801 on acute phase changes induced by partial global cerebral ischemia in mice

2007 ◽  
Vol 172 ◽  
pp. S63
Author(s):  
Amitava Chakrabarti ◽  
Raman Aggarwal ◽  
Bikash Medhi ◽  
Ashis Pathak ◽  
Veena Dhawan
Keyword(s):  
Cerebral Ischemia ◽  
Acute Phase ◽  
Phase Changes ◽  
Global Cerebral Ischemia ◽  
Mk 801

scholarly journals MK-801 (Dizocilpine) Protects the Brain from Repeated Normothermic Global Ischemic Insults in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 925-932 ◽  
Author(s):  
Baowan Lin ◽  
W. Dalton Dietrich ◽  
Myron D. Ginsberg ◽  
Mordecai Y.-T. Globus ◽  
Raul Busto
Keyword(s):  
Cerebral Ischemia ◽  
Repeated Measures ◽  
Neuronal Damage ◽  
Brain Temperature ◽  
Global Cerebral Ischemia ◽  
Striatal Neurons ◽  
Ischemic Insult ◽  
Mk 801 ◽  
Bilateral Carotid ◽  
Ventrolateral Thalamus

We investigated the neuroprotective potential of MK-801 (dizocilpine), a noncompetitive N-methyl-d-aspartate (NMDA) antagonist, in the setting of three 5-min periods of global cerebral ischemia separated by 1-h intervals in halothane-anesthetized rats. Each ischemic insult was produced by bilateral carotid artery occlusions plus hypotension (50 mm Hg). Brain temperature was maintained at normothermic levels (36.5–37.0°C) throughout the experiment. MK-801 (3 mg/kg) (n = 6) or saline (n = 6) was injected intraperitoneally 45 min following the end of the first ischemic insult. Following 7-day survival, quantitative neuronal counts of perfusion-fixed brains revealed severe ischemic damage in hippocampal CA1 area, neocortex, ventrolateral thalamus, and striatum of untreated rats. By contrast, significant protection was observed in MK-801-treated rats. In area CA1 of the hippocampus, numbers of normal neurons were increased 11- to 14-fold by MK-801 treatment (p < 0.01). The ventrolateral thalamus of MK-801-treated rats showed almost complete histologic protection, and neocortical damage was reduced by 71% (p < 0.01). The degree of MK-801 protection of striatal neurons was less complete than that seen in other vulnerable structures, amounting to 63% for central striatum (p = 0.02, Mann–Whitney U test) and 48% in the dorsolateral striatum (NS). A repeated-measures analysis of variance demonstrated a highly significant overall protective effect of MK-801 treatment ( F1,10 = 37.2, p = 0.0001). These findings indicate that excitotoxic mechanisms play a major role in neuronal damage produced by repeated ischemic insults and that striking cerebroprotection is conferred by MK-801 administered following the first insult in animals with cerebral normothermia. NMDA antagonists may prove useful in patients at risk of repeated episodes of cerebral ischemia.

Resveratrol prevents oxidative stress and inhibition of Na+K+-ATPase activity induced by transient global cerebral ischemia in rats

2011 ◽  
Vol 22 (10) ◽  
pp. 921-928 ◽  
Author(s):  
Fabrício Simão ◽  
Aline Matté ◽  
Cristiane Matté ◽  
Flavia M.S. Soares ◽  
Angela T.S. Wyse ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Atpase Activity ◽  
Global Cerebral Ischemia ◽  
Transient Global Cerebral Ischemia

Neutrophil arachidonic acid level and adhesive capability are increased in essential hypertension

1998 ◽  
Vol 16 (5) ◽  
pp. 585-592 ◽  
Author(s):  
Oliviero Olivieri ◽  
Sara Lombardi ◽  
Carla Russo ◽  
Domenico Girelli ◽  
Patrizia Guarini ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Essential Hypertension ◽  
Acid Level ◽  
Arachidonic Acid Level

Arachidonic Acid Level of Non-esterified Fatty Acids and Phospholipids in Serum and Heart Muscle of Patients with Fatal Myocardial Infarction

2009 ◽  
Vol 223 (3) ◽  
pp. 233-238 ◽  
Author(s):  
GUDRUN SKULADOTTIR ◽  
ELSA BENEDIKTSDOTTIR ◽  
THORDUR HARDARSON ◽  
JONAS HALLGRIMSSON ◽  
GUDMUNDUR ODDSSON ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Fatty Acids ◽  
Arachidonic Acid ◽  
Heart Muscle ◽  
Acid Level ◽  
Arachidonic Acid Level ◽  
Esterified Fatty Acids ◽  
Fatal Myocardial Infarction

Alkalemia reduces recovery from global cerebral ischemia by NMDA receptor-mediated mechanism

1997 ◽  
Vol 272 (6) ◽  
pp. H2557-H2562
Author(s):  
P. D. Hurn ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Energy Metabolism ◽  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Nmda Receptor Antagonist ◽  
Global Cerebral Ischemia ◽  
Resonance Spectroscopy ◽  
Mk 801 ◽  
Sagittal Sinus

In vitro data suggest that low tissue pH reduces, whereas extracellular alkalosis potentiates, cerebral anoxic injury via excitotoxic mechanisms. We tested the hypothesis that in vivo metabolic alkalemia potentiates defects in energy metabolism after global incomplete cerebral ischemia (12 min) and reperfusion (180 min) by an N-methyl-D-aspartate (NMDA) receptor-mediated mechanism. Brain ATP, phosphocreatine, and intracellular pH (pHi) were measured by 31P magnetic resonance spectroscopy in anesthetized dogs treated with 1) preischemic intravenous carbicarb buffer (NaHCO3+Na2CO3, Carb, n = 7); 2) carbicarb infusion plus NMDA receptor antagonist MK-801 (MK-801 + Carb, n = 7); 3) an osmotically equivalent volume of 5% NaCl (NaCl, n = 8); or 4) equivalent volume of 0.9% NaCl (Sal, n = 3). Sagittal sinus pH was raised to 7.82 +/- 0.04 before and 7.65 +/- 0.03 during ischemia in Carb vs. 7.72 +/- 0.01 and 7.60 +/- 0.01 in MK-801+Carb, 7.25 +/- 0.02 and 7.15 +/- 0.03 in NaCl, and 7.31 +/- 0.00 and 7.26 +/- 0.01 in Sal, respectively. Ischemic cerebral blood flow (CBF, radiolabeled microspheres), pHi, and ATP reduction were similar among groups. By 180 min of reperfusion, recovery of ATP was greater in MK-801+Carb (104 +/- 6% of baseline), NaCl (93 +/- 6%), and Sal (94 +/- 6%) than in Carb (47 +/- 6%). Intraischemic pHi was similar among groups, and pHi recovery did not vary among groups despite differences in sagittal sinus pH. In Carb, CBF was restored but with delayed hypoperfusion. We conclude that extracellular alkalosis is deleterious to postischemic CBF and energy metabolism, acting by NMDA receptor-mediated mechanisms.

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