Key Points
- To evaluate the effects of beta-adrenergic stimulation and atrial pacing on the transmural distribution of intracellular free adenosine in canine hearts in vivo.
- Assessed in vivo canine hearts during functional hyperemia induced by isoproterenol infusion (0.3–0.5 µg/kg/min iv for 30 min) and atrial pacing (209 ± 4 beats/min).
- Measured intracellular free adenosine accumulation across subepicardial, midmyocardial, and subendocardial layers using S-adenosylhomocysteine (SAH) trapping during continuous homocysteine infusion (1.6 mg/kg/min iv).
- Isoproterenol increased left ventricular dP/dtmax by 86%, heart rate by 38%, and MVO2 by 62%, while diastolic aortic pressure decreased from 107 ± 12 to 58 ± 5 mmHg.
- During beta-adrenergic stimulation, SAH accumulation increased by 1.6-fold in subepicardial, 2.5-fold in midmyocardial, and 4.4-fold in subendocardial layers, showing an inverse relationship with diastolic aortic pressure.
- Atrial pacing at 209 ± 4 beats/min elevated MVO2 by 42% and increased SAH levels by 1.5-, 3.3-, and 1.9-fold in subepicardial, midmyocardial, and subendocardial layers, respectively.
Structured PICO
PPopulationDog hearts in vivo
IInterventionBeta-adrenergic stimulation (isoproterenol 0.3-0.5 micrograms.kg-1.min-1 iv for 30 min) and atrial pacing (209 +/- 4 beats/min)
OOutcomeTransmural gradient of intracellular free adenosine (measured by accumulation of S-adenosylhomocysteine)surrogate
Beta-adrenergic stimulation and pacing cause an inhomogeneous transmural increase in free intracellular adenosine in the in situ canine heart, which is critically dependent on diastolic aortic pressure.