EFFECTS OF TEMPERATURE CHANGE, OXYGEN DEPRIVATION AND CATIONS ON THE ATRIAL RESPONSES TO VAGAL STIMULATION

• Published in: Japanese journal of pharmacology Vol. 14; no. 2; pp. 118 - 137
• Main Authors: TODA, NOBORU, FUJIWARA, MOTOHATSU, SHIMAMOTO, KIRO
• Format: Journal Article
• Language: English
• Published: Japan The Japanese Pharmacological Society 01-01-1964
• Subjects: Acetylcholine; Animals; Barium; Calcium; Cations; Chlorides; Electric Stimulation; Guinea Pigs; Heart; Heart Atria; Hypoxia; Magnesium; Old Medline; Oxygen; Pharmacology; Potassium; Rabbits; Sodium Chloride; Temperature; Vagus Nerve; VAGUS NERVE; ACETYLCHOLINE; GUINEA PIGS; EXPERIMENTAL LAB STUDY; ELECTRIC STIMULATION; HEART; MAGNESIUM; RABBITS; BARIUM; TEMPERATURE; ANOXIA; PHARMACOLOGY; CALCIUM; CHLORIDES; SODIUM CHLORIDE; POTASSIUM
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1254/jjp.14.118

It is generally believed that the cardiac fibers of the right vagus nerve terminate, in large part, near the sinoatrial node and some fibers distribute widely in the atria, and that most of the cardiac fibers of the left vagus supply the atrioventricular node and bundles. On the other hand, there are opposite conclusions regarding the existence of the vagus nerve endings in the ventricles. Electrical stimulation of the vagal fibers to the heart has usually been performed in the open chest animal or in the heart-lung preparation of the dog. Many investigators agree with the inhibitory nature of the vagal innervation on the heart, while there is some evidence for existence of the cardio-accelerator fibers in the vagus nerve (1-4). Middleton et al. (5) have concluded that some vagal fibers make connection with the chromaffin cells or the adrenergic neurons located in or near the heart by demonstrating an adrenaline-like substance in the perfusate of the cat's heart which is responding with the increase in rate and amplitude to vagal stimulation. McEwen (6) has observed an inhibitory effect of vagal stimulation in the rabbit's heart for many hours after the isolation. He, further, has demonstrated that the vagal stimulation restores the normal rhythmicity of contraction in the atria arrested by suspending in the bath for many hours, and that the same vagal stimulation inihibits the regular rhythm restored by the addition of acetylcholine. Using the same type of preparations, Burn and Rand (7) have observed the restarting effect of vagal stimulation on the heart which ceased to beat by cooling. The marked acceleration of the repolarization phase in the atrial membrane potentials of the dog's and rat's hearts in situ following vagal stimulation has been shown by Hoffman and Suckling (8) and Biersteker et al. (9). Similar observation was made on the turtle's heart in situ by Churney et al. (10). Although the vagal effect on the membrane potentials of the isolated frog's heart was demonstrated by Hutter and Trautwein (11), the vagal effect on the atrial or ventricular membrane potentials of the isolated mammalian heart has not hitherto been presented. During the study of the effect of va, al stimulation on the transmembrane potentials (12), the authors have been confronted with many difficulties which should be previously removed in the isolated atrial preparation with the vagal innervation. Accordingly, the present report concerns with the physiological studies on the effects of vagal stimulation on contraction rate and amplitude in the isolated rabbit's and guinea-pig's atria.