Key result
Adenosine-regulating agents depressed AV nodal conduction in a frequency-dependent manner in guinea pig hearts, with SH interval prolongation ratios at fast to slow pacing rates ranging from 3.5 to 17.5.
Why the study?
Do metabolic and allosteric regulators of endogenous adenosine cause event-specific depression of AV nodal conduction in guinea pig hearts?
Do metabolic and allosteric regulators of endogenous adenosine cause event-specific depression of AV nodal conduction in guinea pig hearts?
Adenosine-regulating agents depress AV nodal conduction in a frequency-dependent manner, suggesting potential as a novel strategy for treating supraventricular arrhythmias.
No takes yet. Share an insight, caveat, or question.
Hypothesis-generating for adenosine modulators in supraventricular arrhythmias; human studies needed before any clinical consideration.
Dennis et al. (1996) studied this question. Metabolic and allosteric regulators of endogenous adenosine (ITU, EHNA, draflazine, PD81,723) vs. adenosine and diltiazem was evaluated on stimulus-to-His bundle (SH) interval. Adenosine-regulating agents depressed AV nodal conduction in a frequency-dependent manner in guinea pig hearts, with SH interval prolongation ratios at fast to slow pacing rates ranging from 3.5 to 17.5.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: