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Adenosine decreases the fibrillation threshold in atrial myocardium
J Szegi1, A J Szentmiklósi, A Cseppentö
1Department of Pharmacology, Medical University of Debrecen, Hungary.
Insights
Adenosine significantly lowers the atrial fibrillation threshold and shortens the refractory period in heart tissue. These effects, observed in vivo and in vitro, may contribute to atrial fibrillation during adenosine treatment.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
Background:
- Adenosine is a nucleoside with known effects on cardiac function.
- Understanding adenosine's impact on myocardial electrophysiology is crucial for clinical applications.
Purpose of the Study:
- To investigate the effects of adenosine on atrial and ventricular myocardium.
- To elucidate the electrophysiological mechanisms underlying adenosine-induced cardiac changes.
Main Methods:
- In vivo studies on anesthetized cats.
- In vitro experiments on isolated atrial and ventricular myocardium.
- Measurement of fibrillation threshold, refractory period, diastolic threshold, and contractile force.
Main Results:
- Adenosine decreased the atrial fibrillation threshold and electric diastolic threshold.
- Adenosine shortened the functional refractory period in atrial myocardium, more prominently in guinea-pig left atria.
- Adenosine reduced atrial contractile force; ventricular myocardium was unaffected.
- Aminophylline antagonized adenosine's effects on the functional refractory period.
Conclusions:
- Adenosine alters atrial electrophysiological parameters, potentially contributing to atrial fibrillation.
- These findings suggest a role for adenosine in the pathomechanism of atrial fibrillation observed in patients and dogs.
- Ventricular myocardium appears less sensitive to adenosine's electrophysiological effects.
Abstract:
The action of adenosine on the fibrillation threshold, effective refractory period, electric diastolic threshold and mechanical activity of the atrial and ventricular myocardium was studied in vivo and in vitro. In anaesthetized, open-chest cats, the atrial fibrillation threshold significantly decreased under adenosine-infusion (1 mumols/kg/min). In electrically stimulated atrial myocardium of cats, adenosine (10 mumols/l-1 mmol/l) was capable of evoking a concentration-dependent decrease in electric diastolic threshold and shortening the functional refractory period. Adenosine decreased also the contractile force. The shortening on the functional refractory period was more prominent in electrically driven guinea-pig left atrial myocardium. This action could be antagonized by aminophylline, a competitive antagonist on P1 purinoceptors. In ventricular myocardium, adenosine did not influence the fibrillation threshold, the electric diastolic threshold, the functional refractory period or contractile force. On the basis of these observations it can be assumed that the above changes in the extracellular electrophysiological parameters may play a role in the pathomechanism of atrial fibrillation occasionally manifested during treatment with adenosine in patients as well as in dogs.