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Published on: April 19, 2011
Ischemic preconditioning - an opiate constitutive nitric oxide molecular hypothesis
G B Stefano1, K Neenan, P Cadet
1Neuroscience Research Institute, State University of New York College at Old Westbury, Old Westbury, New York 11568, USA. stefanog@surg.som.sunysb.edu
Summary
Transient ischemia may protect the heart by mimicking exercise responses. This process, involving nitric oxide, down-regulates cellular activity, offering protection against sustained cardiac insults.
Area of Science:
- Cardiovascular Physiology
- Cellular Signaling
Background:
- Coronary artery disease is the leading cause of adult mortality in the US.
- Transient ischemia is being investigated for its potential to precondition the myocardium.
- Myocardial preconditioning may involve endogenous physiological processes.
Purpose of the Study:
- To review the speculative role of ischemic preconditioning in protecting the myocardium.
- To propose that ischemic preconditioning is linked to physiological processes associated with exercise.
- To explore the involvement of nitric oxide, opiates, and opioids in myocardial protection.
Main Methods:
- Speculative review of existing literature.
- Analysis of cellular responses to transient ischemia and metabolic demand.
- Examination of signaling pathways involving nitric oxide synthase, opiates, and opioids.
Main Results:
- Transient ischemia mimics cellular responses to normal metabolic ATP dips.
- Constitutive nitric oxide synthase-derived nitric oxide down-regulates cellular excitatory states.
- Opiate and opioid signaling may contribute to protection by releasing nitric oxide.
Conclusions:
- Ischemic preconditioning protection likely arises from an existing physiological process linked to exercise.
- Endogenous nitric oxide stimulators protect by engaging a process that limits activation after physical exertion.
- Nitric oxide plays a key role in dampening cellular activity for protection against ischemic insults.
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