Key result
Aminoguanidine significantly decreased iNOS activity (1.04 vs 29.1 pmol/min/mg protein, P<0.01) and improved hemodynamic parameters in rats with experimental autoimmune myocarditis.
Why the study?
Does aminoguanidine improve hemodynamics and attenuate histopathological changes in a rat model of experimental autoimmune myocarditis?
Population
Lewis rats immunized with cardiac myosin (animal model of experimental autoimmune myocarditis)
Comparison
Aminoguanidine (a selective inhibitor of iNOS) vs Untreated myosin-immunized rats
Design
Preclinical
Follow-up
Up to 49 days
Authors
Loading...
iNOS role in EAM hypothesis-generating; leaves open contribution to human myocarditis.
Does aminoguanidine improve hemodynamics and attenuate histopathological changes in a rat model of experimental autoimmune myocarditis?
Absolute Event Rate: 1.04% vs 29.1%
p-value: p=< .01
Inhibition of iNOS with aminoguanidine attenuates histopathological changes and improves cardiac hemodynamics in a rat model of experimental autoimmune myocarditis, suggesting NO plays a key pathophysiological role.
Hirono et al. (1997) studied Experimental autoimmune myocarditis. Aminoguanidine vs. Untreated myosin-immunized rats was evaluated on iNOS activity (pmol.min-1.mg protein-1) on day 21 (p=< .01). Aminoguanidine significantly decreased iNOS activity (1.04 vs 29.1 pmol/min/mg protein, P<0.01) and improved hemodynamic parameters in rats with experimental autoimmune myocarditis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: