Why the study?
Does m-AMSA affect inotropy and refractoriness in the rat isolated heart model?
Does m-AMSA affect inotropy and refractoriness in the rat isolated heart model?
m-AMSA demonstrates acute moderate negative inotropic effects and prolongs refractoriness in isolated rat hearts, suggesting membranal cardiotoxicity.
May signal cardiotoxicity risk with m-AMSA; hypothesis-generating for human cardiac effects.
m-AMSA (4'[9-acridinylamino]methansulphon-m-anisidide) is a new cytoxic agent now under clinical trial. We used the rat isolated perfused heart model in order to investigate the cardiac effects of m-AMSA. The results of the dose-response study indicate that m-AMSA has an acute moderate negative inotropic effect. The 90% effect (25% decrease in developed force compared to the control) was observed at drug concentration of 1.5 micrograms/ml. The refractory period (as measured by stimuli of twice diastolic threshold intensity) increased progressively as the drug concentration was increased (up to 2.5 micrograms/ml). Measurements of the strength-duration and strength-interval relationship showed that m-AMSA induced a significant reduction (P less than 0.005) in excitability and prolongation of refactoriness. We suggest that m-AMSA has a membranal cardiotoxic effect in addition to its known intracellular cytotoxic effect.
No takes yet. Share an insight, caveat, or question.
MERKIN et al. (1985) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: