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Enhanced iNOS function in myocytes one day after brief ischemic episode
Song-Jung Kim1, Young-Kwon Kim, Gen Takagi
1Cardiovascular Research Institute and Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103, USA. kimso@umdnj.edu
American Journal of Physiology. Heart and Circulatory Physiology
|January 15, 2002
Summary
A brief heart ischemia episode enhances nitric oxide (NO) production via inducible NO synthase (iNOS) in cardiac cells and surrounding areas. This iNOS upregulation is key for heart protection during the "second window of protection" (SWOP).
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Biomedical Science
Background:
- Nitric oxide (NO) from inducible NO synthase (iNOS) is implicated in cardiac protection during the
- second window of protection
- (SWOP).
- Understanding the role and localization of iNOS in cardiac myocytes during SWOP is crucial for developing cardioprotective strategies.
Purpose of the Study:
- To investigate if transient ischemia enhances NOS function in cardiac myocytes.
- To identify the specific NOS isoform responsible for this enhanced function.
- To determine the spatial expression of iNOS during SWOP.
Main Methods:
- Induction of regional myocardial ischemia (10-min coronary artery occlusion) in dogs, followed by 24-h reperfusion.
- Isolation of cardiac myocytes from ischemic and non-ischemic regions for contractile function assessment.
- Inhibition studies using non-specific and specific NOS inhibitors (N(G)-nitro-L-arginine, 2-amino-5,6-dihydro-6-methy-4H-1,3-thiazine).
- Immunohistochemical analysis to localize iNOS expression.
Main Results:
- Transient ischemia significantly enhanced NOS-dependent myocyte contraction in the ischemic region, but not the non-ischemic region.
- This enhanced contraction was specifically mediated by iNOS, as it was abolished by a specific iNOS inhibitor.
- Immunohistochemistry revealed increased iNOS expression in the myocardium and interstitial spaces of the ischemic zone.
Conclusions:
- A transient ischemic episode upregulates iNOS function in cardiac myocytes.
- Enhanced iNOS expression occurs in both myocytes and the interstitial space, suggesting a strategic role in cardioprotection.
- These findings highlight iNOS as a critical mediator of cardiac protection during the SWOP.