Chemical Preconditioning with 3-Nitropropionic Acid in Gerbil Hippocampal Slices: Therapeutic Window and the Participation of Adenosine Receptor

Aketa, Shuta; Nakase, Hiroyuki; Kamada, Yoshitaka; Hiramatsu, Kazuhiro; Sakaki, Toshisuke

doi:10.1006/exnr.2000.7507

Cited by 19 publications

(9 citation statements)

References 40 publications

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“…3-NP (Sigma, St Louis, MO) was dissolved in distilled water at 1 mg/ml (pH 7.4, adjusted with NaOH). A single subtoxic dose of 3-NP (20 mg/kg, [8]) was applied intraperitoneally as described previously [11]. After isolation of the hearts, 10 min stabilization period, 30 min aerobic perfusion, 30 min global ischemia, and 120 min reperfusion were applied as in the non-treated control group.…”

Section: Experimental Groupsmentioning

confidence: 99%

“…The term chemical preconditioning was used first by Riepe and Ludolph [8] for the induction of hypoxic tolerance by using 3-nitropropionic acid in the brain. Other studies also suggested that the application of 3-NP in a single dose up to 20 mg/kg is a suitable strategy to induce chemical preconditioning with an early onset and long duration in the brain [8,11], (see Ref. [12] for review).…”

Section: Introductionmentioning

confidence: 99%

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The role of peroxynitrite in chemical preconditioning with 3-nitropropionic acid in rat hearts

Turan

Csonka

Csont

et al. 2006

Cardiovascular Research

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Section: Experimental Groupsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The role of peroxynitrite in chemical preconditioning with 3-nitropropionic acid in rat hearts

Turan

Csonka

Csont

et al. 2006

Cardiovascular Research

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“…For typical studies using test occlusions of 6-10 mins (Dave et al, 2001;Kato et al, 1995;Shamloo and Wieloch, 1999), delayed depolarization would therefore achieve at least 10% and perhaps as much as 25% reductions in effective insult severity. Interestingly, chemical preconditioning by in vivo pretreatment of gerbils with 3-nitropropionic acid was found to delay depolarization in hippocampal slices during subsequent hypoxia in vitro (Aketa et al, 2000), indicating the potential heterogeneity in factors contributing to protection across preconditioning treatments within a given species. Mechanisms responsible for the observed depolarization delay remain to be identified.…”

Section: Changes In Depolarization Kinetics Associated With Preconditmentioning

confidence: 99%

Protective Preconditioning by Transient Global Ischemia in the Rat: Components of Delayed Injury Progression and Lasting Protection Distinguished by Comparisons of Depolarization Thresholds for Cell Loss at Long Survival Times

Ueda

Nowak²

2005

J Cereb Blood Flow Metab

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Robust ischemic preconditioning has been shown in rodent brain, but there are concerns regarding the persistence of neuron protection. This issue was examined in rat hippocampus following 4-vessel occlusion (4-VO) ischemia, using DC shifts characteristic of ischemic depolarization to reproducibly define insult severity. Preconditioning ischemia producing 2 to 3.5 mins depolarization was followed at intervals of 2, 5, or 7 days by test insults of varied duration, after which CA1 counts were obtained at 1, 2, 4, or 12 weeks. Neuron loss in naive animals increased with depolarization time longer than 4 mins regardless of postischemic survival interval. Preconditioning 2, 5, or 7 days before test insults prolonged the injury threshold evaluated at 1 week survival to 15, 9, or 6 mins, respectively, showing robust protection and a rapid decay of the protected state. However, by 2 weeks survival after preconditioning at a 2-day interval, the injury threshold dramatically regressed from 15 to 9 mins. Thereafter protection remained relatively stable through 1 month, but slight progression of neuron injury was evident at 3 months. Inflammatory responses were seen in both naive and preconditioned hippocampi throughout this interval, appropriate to the extent of neuron injury. These studies show distinct components of transient and lasting protection after ischemic preconditioning. Finally, it was found that ischemic depolarization was delayed by approximately 1 min in optimally preconditioned rat hippocampus, in contrast to previous results in the gerbil, identifying one specific mechanism by which insult severity is reduced in this model.

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“…Adenosine receptor activation (Aketa et al, 2000), opening of mitocondrial K ATP channels , releasing of free radical (Wiegand et al, 1999), or increase in the ratio of bcl/ bax (Brambrink et al, 2000) has been previously shown to be the mechanism(s) of late -preconditioning in cerebral ischemia-reperfusion models. However, the mechanism of 3-NP induced-late preconditioning has not been investigated in the isolated rat heart.…”

Section: Discussionmentioning

confidence: 98%

“…On the other hand, a single low dose of 3-NP (up to 20 mg/kg) has been shown to increase ischemic tolerance in rat brain without producing any histological lesions Sugino et al, 1999;Wiegand et al, 1999). Aketa et al (2000) have shown that 3-NP induced preconditioning has an early onset (3h) and long lasting (24 h) protective effect. Similarly, Zhu et al (2004) showed that 3-NP (20 mg/kg, i.p) reduced infarct volume in cerebellum after 3 days of its injection.…”

Section: Introductionmentioning

confidence: 98%

The mechanism of the late preconditioning effect of 3-nitropropionic acid

et al. 2008

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The aim of the present study was to investigate the mechanism of effect of 3-nitropropionic acid-(3-NP) induced late preconditioning in rat heart. For this purpose 20-30 min before 3-NP (20 mg/kg, i.p.) injection, the rats were treated intraperitoneally with 5-hydroxydecanoate (40 mg/kg, 5-HD, mitochondrial K(ATP)-channel blocker), L-NAME (100 mg/kg, NOS inhibitor), N-2-mercaptopropionylglycine (100 mg/kg, MPG, free radical scavenger), or superoxide dismutase+catalase (10000+10000 IU/kg, SOD+CAT). Control rats received saline only without 3-NP pretreatment. After two days, hearts were isolated and perfused at a constant pressure in a Langendorff apparatus. 15-min global ischemia followed by 30-min reperfusion was applied to all hearts. Pretreatment of 3-NP significantly reduced infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) levels, and incidence of ventricular tachycardia (VT) compared with the control group receiving saline only. 5-HD, L-NAME, MPG, or SOD+CAT treatment statistically reversed 3-NP-induced reduction in infarct size. Although CK-MB, LDH levels, and incidence of VT were also reduced by L-NAME, MPG, or SOD+CAT treatment, only 5-HD significantly inhibited beneficial effects of 3-NP on all of the parameters above. These results showed that mito-K(ATP) channels play a pivotal role in late preconditioning effect of 3-NP in the isolated rat heart. However, other mediators such as reactive oxygen species and NO may be, at least in part, involved in mechanisms of this effect.

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Chemical Preconditioning with 3-Nitropropionic Acid in Gerbil Hippocampal Slices: Therapeutic Window and the Participation of Adenosine Receptor

Cited by 19 publications

References 40 publications

The role of peroxynitrite in chemical preconditioning with 3-nitropropionic acid in rat hearts

The role of peroxynitrite in chemical preconditioning with 3-nitropropionic acid in rat hearts

Protective Preconditioning by Transient Global Ischemia in the Rat: Components of Delayed Injury Progression and Lasting Protection Distinguished by Comparisons of Depolarization Thresholds for Cell Loss at Long Survival Times

The mechanism of the late preconditioning effect of 3-nitropropionic acid

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