August 1, 2003The FASEB Journal
Up‐regulation of cardiac nitric oxide synthase 1‐derived nitric oxide after myocardial infarction in senescent rats
Key result
Myocardial infarction in senescent rats increased cardiac NOS1 expression and activity, counteracting decreased NOS3 activity and playing a significant role in regulating myocardial contractility.
Why the study?
Does preferential in vivo inhibition of NOS1 activity worsen left ventricular dysfunction in senescent rats after myocardial infarction?
Population
Senescent rats with an experimental model of myocardial infarction (MI)
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Hypothesis-generating for NOS1 compensation in aged post-MI hearts; prospective human studies needed before clinical consideration.
Structured PICO
Does preferential in vivo inhibition of NOS1 activity worsen left ventricular dysfunction in senescent rats after myocardial infarction?
P
Population
Senescent rats with an experimental model of myocardial infarction (MI)
I
Intervention
Preferential in vivo inhibition of NOS1 activity
O
Outcome
Cardiac NOS1 expression and activity, and left ventricular dysfunctionsurrogate
Increased NOS1-derived NO production plays a significant role in the autocrine regulation of myocardial contractility after myocardial infarction in aging rats.
Cite This Study
Damy et al. (2003) studied Myocardial infarction. In vivo inhibition of NOS1 activity was evaluated on Cardiac NOS1 expression and activity, and left ventricular dysfunction. Myocardial infarction in senescent rats increased cardiac NOS1 expression and activity, counteracting decreased NOS3 activity and playing a significant role in regulating myocardial contractility.