Moderate hypothermia mitigates neuronal damage in the rat brain when initiated several hours following transient cerebral ischemia

1994 ◽  
Vol 87 (4) ◽  
pp. 325-331 ◽  
Author(s):  
Cicero Coimbra ◽  
Tadeusz Wieloch
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia ◽  
Moderate Hypothermia

scholarly journals In Vivo Microdialysis of Endogenous and 13C-labeled TCA Metabolites in Rat Brain: Reversible and Persistent Effects of Mitochondrial Inhibition and Transient Cerebral Ischemia

Metabolites ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 204 ◽  
Author(s):  
Jesper F. Havelund ◽  
Kevin H. Nygaard ◽  
Troels H. Nielsen ◽  
Carl-Henrik Nordström ◽  
Frantz R. Poulsen ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mitochondrial Dysfunction ◽  
Rat Brain ◽  
De Novo ◽  
Tricarboxylic Acid Cycle ◽  
Experimental Models ◽  
Transient Cerebral Ischemia ◽  
Metabolic Disturbances ◽  
Metabolic Marker

Cerebral micro-dialysis allows continuous sampling of extracellular metabolites, including glucose, lactate and pyruvate. Transient ischemic events cause a rapid drop in glucose and a rise in lactate levels. Following such events, the lactate/pyruvate (L/P) ratio may remain elevated for a prolonged period of time. In neurointensive care clinics, this ratio is considered a metabolic marker of ischemia and/or mitochondrial dysfunction. Here we propose a novel, sensitive microdialysis liquid chromatography-mass spectrometry (LC-MS) approach to monitor mitochondrial dysfunction in living brain using perfusion with 13C-labeled succinate and analysis of 13C-labeled tricarboxylic acid cycle (TCA) intermediates. This approach was evaluated in rat brain using malonate-perfusion (10–50 mM) and endothelin-1 (ET-1)-induced transient cerebral ischemia. In the malonate model, the expected changes upon inhibition of succinate dehydrogenase (SDH) were observed, i.e., an increase in endogenous succinate and decreases in fumaric acid and malic acid. The inhibition was further elaborated by incorporation of 13C into specific TCA intermediates from 13C-labeled succinate. In the ET-1 model, increases in non-labeled TCA metabolites (reflecting release of intracellular compounds) and decreases in 13C-labeled TCA metabolites (reflecting inhibition of de novo synthesis) were observed. The analysis of 13C incorporation provides further layers of information to identify metabolic disturbances in experimental models and neuro-intensive care patients.

Dissecting functional phenotypes of microglia and macrophages in the rat brain after transient cerebral ischemia

Glia ◽  
2018 ◽  
Vol 67 (2) ◽  
pp. 232-245 ◽  
Author(s):  
Wenson D. Rajan ◽  
Bartosz Wojtas ◽  
Bartlomiej Gielniewski ◽  
Anna Gieryng ◽  
Malgorzata Zawadzka ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Transient Cerebral Ischemia

scholarly journals Accelerated and Exacerbated Effects of High Dietary Fat on Neuronal Damage Induced by Transient Cerebral Ischemia in the Gerbil Septum

2014 ◽  
Vol 29 (3) ◽  
pp. 328 ◽  
Author(s):  
Seung Hwan Cheon ◽  
Bing Chun Yan ◽  
Bai Hui Chen ◽  
Joon Ha Park ◽  
Ji Hyeon Ahn ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Dietary Fat ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia

scholarly journals Postischemic Blockade of AMPA but Not NMDA Receptors Mitigates Neuronal Damage in the Rat Brain following Transient Severe Cerebral Ischemia

1992 ◽  
Vol 12 (1) ◽  
pp. 2-11 ◽  
Author(s):  
B. Nellgård ◽  
T. Wieloch
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Ampa Receptor ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia ◽  
Coupled Processes ◽  
Temporal Part ◽  
Nmda Receptor Antagonists ◽  
Receptor Antagonists ◽  
Cgp 40116

Glutamatergic transmission is an important factor in the development of neuronal death following transient cerebral ischemia. In this investigation the effects of N-methyl-d-aspartate (NMDA) and non-NMDA receptor antagonists on neuronal damage were studied in rats exposed to 10 min of transient cerebral ischemia induced by bilateral common carotid occlusion combined with hypotension. The animals were treated with a blocker of the ionotropic quisqualate or α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor, 2.3-dihydroxy-6-nitro-7-sulfamoyl-benzo( F)quinoxaline (NBQX), given postischemia as an intraperitoneal bolus dose of 30 mg kg−1 followed by an intravenous infusion of 75 μg min−1 for 6 h, or with the noncompetitive NMDA receptor blocker dizocilpine(MK-801) given 1 mg kg−1 i.p. at recirculation and 3 h postischemia, or with the competitive NMDA receptor antagonist dl-( E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 40116), 5 mg kg−1, given intraperitoneally at recirculation. Treatment with NBQX provided a significant reduction of neuronal damage in the hippocampal CA1 area by 44–69%, with the largest relative decrease in the temporal part of the hippocampus. In neocortex a significant decrease in the number of necrotic neurons was also noted. No protection could be seen following postischemic treatment with dizocilpine or CGP 40116. Our data demonstrate that AMPA but not NMDA receptor antagonists decrease neuronal damage following transient severe cerebral ischemia in the rat and that the protection by NBQX may be dependent on the severity of the ischemic insult. We propose that the AMPA receptor–mediated neurotoxicity could be due to ischemia-induced changes in the control mechanisms of AMPA receptor–coupled processes or to changes of AMPA receptor characteristics.

Effects of transient cerebral ischemia on hsp40 mRNA levels in rat brain

1998 ◽  
Vol 55 (2) ◽  
pp. 341-344 ◽  
Author(s):  
Wulf Paschen ◽  
Thomas Linden ◽  
Jens Doutheil
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Transient Cerebral Ischemia ◽  
Mrna Levels
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