Effect of Aminophylilne on the Adenosine-induced Decrease in Sinus Rate .
10.4097/kjae.1986.19.1.71
- Author:
Wha Ja KANG
1
;
Kwang II SHIN
Author Information
1. Department of Anesthesiology, Medical School, Kyung-Hee University, Seoul, Korea.
- Publication Type:Original Article
- MeSH:
Acetylcholine;
Action Potentials;
Adenosine;
Aminophylline;
Cell Membrane;
Dipyridamole;
Fires;
Heart;
Humans;
Membranes;
Research Personnel
- From:Korean Journal of Anesthesiology
1986;19(1):71-83
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Since the first report by Drury and Szent-Gyorgyi in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. A lot of investigations on the working mechanisms of adenosine have been focused mainly on the effects on the coronary blood flow. However, the cellular mechanisms underlyiag the inhibitory action of adenosine on the SA node are not well understood yet. Furthe-rmore, the physiological role of adenosine in the regulation of the heart beat remains still to be explored. Thus, this study was undertaken to examine the behavior of the rabbit SA node ander the influence of adenosine, and the interactions between adenosine and aminophylline on the SA node, and then to compare these results with those of acetylcholine. At the same dosage range, adenosine suppressed the sinus rate and atrial contractility even in the reserpinized preparation. The spontaneous firing rate of the SA node at 35degrees C (mean+/-SEM, n=16) was 154+/-3.3 beats/min. The parameters of action potential were: maximum diastolic potential(MDP), -73+/-1,7 mV; overshoot(OS), 9+/-1.4 mV; slope of pacemaker potential(SPP), 94+/-3.0 mV/sec. Adenosine suppressed the firing rate of the SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of 10(-4)M and was potentiated in parallel with the increase in adenosine concentration. Changes in the action potential by adenosine were dose-dependent as show by the increase of MDP and the decrease of SPP until 10(-4)M. Above this concentration, however, the amplitude of the action potential decreased markedly due to the simultaneous decrease of both MDP and OS. Dipyridamole, which is known to block the adenosine transport aross the cell membrane, definately potentiated the action of adenosine. The effects of adenosine on the SA node were inhibited by aminophylline. However, the similar effects of acetylcholine to those of adenosine were not reversed by aminophylline. These results suggest that adenosine suppressed the pacemaker activity by acting dire-ctly on the membrane of the SA node, and the effects of adenosine on SA node are sele-ctively inhibited by aminophylline.
