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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Social Networks
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. Hosting Providers
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We began analyzing https://journals.physiology.org/doi/10.1152/ajpheart.00678.2003, but it redirected us to https://journals.physiology.org/doi/10.1152/ajpheart.00678.2003. The analysis below is for the second page.

Title[redir]:
Preconditioning protects by inhibiting the mitochondrial permeability transition | American Journal of Physiology-Heart and Circulatory Physiology | American Physiological Society
Description:
Mitochondrial permeability transition (mPT) is a crucial event in the progression to cell death in the setting of ischemia-reperfusion. We have used a model system in which mPT can be reliably and reproducibly induced to test the hypothesis that the profound protection associated with the phenomenon of myocardial preconditioning is mediated by suppression of the mPT. Adult rat myocytes were loaded with the fluorescent probe tetramethylrhodamine methyl ester, which generates oxidative stress on laser illumination, thus inducing the mPT (indicated by collapse of the mitochondrial membrane potential) and ATP depletion, seen as rigor contracture. The known inhibitors of the mPT, cyclosporin A (0.2 μM) and N-methyl-4-valine-cyclosporin A (0.4 μM), increased the time taken to induce the mPT by 1.8- and 2.9-fold, respectively, compared with control (P < 0.001) and rigor contracture by 1.5-fold compared with control (P < 0.001). Hypoxic preconditioning (HP) and pharmacological preconditioning, using diazoxide (30 μM) or nicorandil (100 μM), also increased the time taken to induce the mPT by 2.0-, 2.1-, and 1.5-fold, respectively (P < 0.001), and rigor contracture by 1.9-, 1.7-, and 1.5-fold, respectively, compared with control (P < 0.001). Effects of HP, diazoxide, and nicorandil were abolished in the presence of mitochondrial ATP-sensitive K+ (KATP) channel blockers glibenclamide (10 μM) and 5-hydroxydecanoate (100 μM) but were maintained in the presence of the sarcolemmal KATP channel blocker HMR-1098 (10 μM). In conclusion, preconditioning protects the myocardium by reducing the probability of the mPT, which normally occurs during ischemia-reperfusion in response to oxidative stress.

Matching Content Categories {📚}

  • Fitness & Wellness
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Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

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🌟 Strong Traffic: 100k - 200k visitors per month


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How Does Doi.org Make Money? {💸}

We find it hard to spot revenue streams.

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Keywords {🔍}

mpt, mitochondrial, time, preconditioning, induce, oxidative, stress, diazoxide, channel, rigor, contracture, fig, cell, pharmacological, shown, mitochondria, glibenclamide, membrane, fluorescence, mkatp, tmrm, effect, myocytes, presence, signal, journal, ischemiareperfusion, model, hypoxic, cells, depolarization, american, death, protection, inducing, nicorandil, hmr, function, csa, treatment, physiology, myocardium, ischemic, calcium, buffer, setting, potential, effects, ros, dye,

Topics {✒️}

modified calcium-free krebs-ringer-hepes american physiological society male sprague-dawley rats 585-nm long-pass filter 505-nm long-pass filter voltage-dependent anion channel phototoxicity-induced mitochondrial depolarization physiological genomics journal n-methyl-4-valine-csa n-methyl-4-valine-csa] aps website aps member laser-induced oxidative stress n-methyl-4-valine-cyclosporin journals quick search download figuredownload powerpoint received humane care mediate preconditioning-type protection metabolism american journal reperfusion-induced cell injury reperfusion-induced cell death authors failed global mitochondrial depolarization katp channel blockers tetramethylrhodamine methyl ester mediating preconditioning-induced protection mitochondrial permeability transition applied physiology journal initiate myocardial preconditioning electron transport chain physiology-lung cellular adult rat myocytes generates oxidative stress oxidative stress generated mitochondrial respiratory function inorganic phosphate load molecular probes europe 543-nm emission line 488-nm emission line fluorescent bands orientated include oxidative stress generate oxidative stress outer mitochondrial membrane confocal fluorescence microscopy confocal fluorescence imaging specific mitochondrial signal confocal imaging system putative mkatp channel mitochondrial membrane potential worthington type ii

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External Links {🔗}(518)

Analytics and Tracking {📊}

  • Crazy Egg
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Libraries {📚}

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Mail Servers:

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CDN Services {📦}

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