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Oxidative stress in disease : cardiac ischemia/reperfusion injury / Jay L. Zweier.
- Format:
- Video
- Author/Creator:
- Zweier, Jay L., author.
- Language:
- English
- Subjects (All):
- Free radicals (Chemistry).
- Oxidative stress.
- Physical Description:
- 1 streaming video file (43 min.) : color, sound
- Other Title:
- Oxidative stress in disease
- Place of Publication:
- London : Henry Stewart Talks Ltd, 2007.
- System Details:
- video file
- Summary:
- Audio-visual presentation: Reperfusion injury -- Oxygen radicals are mediators of injury -- Reperfusion radical generation and duration of ischemia -- SOD1 and reperfusion -- Xanthine oxidase as a source of radical generation -- Xanthine oxidase substrates are formed during ischemia -- Superoxide and adhesion molecule expression -- Post-ischemic injury and leukocytes -- NO generation during ischemia -- NO-heme complexes in ischemic heart -- Maximizing myocardial salvage -- EPR imaging.
- Contents:
- Introduction
- Anterior wall myocardial infraction
- Establish early reperfusion
- Reperfusion injury
- Mechanisms of reperfusion injury
- Oxygen radicals are central mediators of injury
- Free radicals in biology
- Evidence for the role of oxygen radicals in injury
- Pressure recovery after ischemia and reperfusion
- Treatment with hSOD in vivo
- Electron paramagnetic/spin resonance
- 5,5-dimethyl-1-pyrroline N-oxide (DMPO)
- EPR spin trapping experiment
- Ischemic duration with maximum radical formation
- Radical generation depends on ischemic duration
- Treatment with active and inactive SOD
- SOD1 over-expression prevents reperfusion injury
- Reoxygenated endothelial cells generate radicals
- Xanthine oxidase - a source of radical generation
- XO and XDH are present in the heart
- XO substrates are formed during ischemia
- EPR spin trapping of endothelial cells and hearts
- Superoxide and functional adhesion
- Superoxide affects adhesion molecule expression
- Superoxide activates leukocyte adhesion
- Role of neutrophils and plasma factors in injury
- Leukocytes and complement enhance injury
- Leukocytes, complement and radical generation
- Leukocytes, complement and injury - conclusions
- Cellular mechanisms of radical generation
- Important biological radicals
- The reaction catalyzed by NO synthase (NOS)
- NOS activity in L-arginine-depleted cells
- N-methyl-D-glucamine dithiocarbamate (MGD)
- EPR spectra of nitric oxide in MGD labeled hearts
- Time course of NO generation during ischemia
- NO generation in the ischemic heart
- Imaging of nitric oxide in the rat heart
- NO-heme complexes formation in ischemic heart
- Myocardial salvage in acute myocardial infarction
- How can we translate this to the clinic?
- Low molecular weight SOD-mimetic (M40403)
- Methods
- Progression of infarct size over time
- Adjusted mean values for infract size
- SOD-mimetic (M40403) study - conclusions
- EPR imaging system setup
- EPR imaging
- EPR imaging of oxygen
- EPR imaging of redox state
- Conclusions
- Acknowledgments
- The OSU heart center.
- Notes:
- Description based on publisher supplied metadata and other sources.
- Retrieved April 17, 2024, from https://hstalks.com/bs/777/.
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