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/.