Über positiv dromotrope Wirkungen von Acetylcholin am Froschherzstreifen

Rothschuh, K. E.; Bammer, Hans

doi:10.1007/bf02047864

Cited by 11 publications

(1 citation statement)

References 12 publications

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“…On the other hand, in the case of the arrest with quinidine, the latter is the more important effect. Evidence has been presented by many workers indicating that quinidine depresses the conduction velocity of heart (13, 30-33), while acetylcholine increases it (32)(33)(34)(35). At least the stimulant action of acetylcholine on the heart arrested by cooling and quinidine might be primarily related to its indirect or direct facilitatory action on the conduction velocity, although the role of the endogenously pro duced acetylcholine played in maintaining the rhythmic contraction of the heart may be of importance.…”

Section: Effect Of Quinidine and Procaine Amide On Cellular Potementioning

confidence: 99%

The Effect of Drugs on the Cardiac Membrane Potentials in the Rabbit

Matsumura

Takaori

1959

Japanese Journal of Pharmacology

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Using the ultramicroelectrode method developed by Ling and Gerard (1), Trautwein et al. (2) and Coraboeuf and Weidmann (3) have recorded slow diastolic depolarization from the pacemaker areas in isolated Purkinje fibers displaying spontaneous beats . Such electrical patterns of spontaneous activity have subsequently been recorded from all cardiac pace makers studied by the intracellular microelectrode method. It is believed that the slow diastolic depolarization is responsible for the intrinsic rhythmicity of the sinus venosus of the frog heart (4-7), the sinus venosus of the turtle heart (8), the sinoatrial node of the rabbit heart (9), ectopic atrial pacemakers in the dog heart (10) and Purkinje fiber pace makers from different mammals (2,3,(11)(12)(13)(14).Observations on the effects of drugs on pacemaker areas of single cardiac muscle fibers would greatly contribute to the clarification of their action to a degree hitherto unattain able by conventional method, but until recently there have been very few reports regarding the effect of drugs on the intracellulary recorded membrane potentials of pacemaker areas. West et al. (9,15) described the use of the ultramicroelectrode technique in localizing and recording from the sinoatrial node of the rabbit atria , and recorded the change in confi guration of the pacemaker potentials as a result of rate modification either by acetylcholine or epinephrine.The present report was designed to record the changes in configuration of the pace maker potentials in the sinoatrial node of the isolated spontaneously beating rabbit atria after the application of a chelating agent, aconitine and antiarrhythmic agents . METHODSThe atria of rabbits were prepared for recording according to the methods described by West (9). The right atrium was suspended horizontally in a lucite chamber of appro ximately 10 c.c. capacity within a constant temperature bath. This was so adjusted that the temperature of the muscle chamber remained at approximately 30'C, which was pre ferred because of a reduction in movement of the preparations. The nutrient solution used in the previous experiments (16) was allowed to flow through a glass warming coil in the water bath and aerated with 100% 0, in a chamber separated from the muscle

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Section: Effect Of Quinidine and Procaine Amide On Cellular Potementioning

confidence: 99%