犬心房の興奮性に關する實驗的研究

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In spite of the numerous experimental studies on the excitability of the auricular muscle since Adrian's experiments in 1920,its relation to the mechanism for the genesis of auricular fibrillation has not been investigated in detail. The author studied the excitability of auricular muscles in dogs with particular emphasis to the change in excitability in anoxia and its relation to the genesis of auricular fibrillation. This study also included some observations on the atrio-ventricular conduction system and its reactions to anoxia.The dog was anesthetized with 10 per cent Oltopan Sodium I. V. and under artificial respiration the chest was opened and the heart was exposed. A bipolar electrode, each terminal of which was made of 100 micron insulated copper wire, was used. To provide each terminal with an arrow-head, approximately 1 mm. at the end of each wire was bent back at about a 30 degree angle and held in position with a drop of solder placed between the bent part and the main wire. The bipolar electrode, each terminal of which was protected by threading it through a 25 gauge injection needle, was thrust through the auricular wall and after the needle was withdrawn, the arrow-heads held the terminals securely at the endocardial surface. An electronic stimulator and a synchronizer were used in combination in order to deliver square wave pulses as stimuli in such a way that the interval between normal and extrasystolic beat as well as voltage and pulse duration could be varied at will. For recording, a three channel oscillograph and a dual beam cathode ray oscilloscope were employed to make a simultaneous recording of the auricular wave and stimulating wave. The experiments were done under normal sinus rhythm except a few cases where electric heart driving was substituted. Results in both instances were essentially the same. Anoxia was obtained by forcing the animal to breathe through an artificial respirator for 10 minutes, a mixture of 10 vol. per cent oxygen and nitrogen or 5 vol. per cent oxygen and nitrogen. Arterial O_2 saturation was determined by the Van Slyke's manometer to check the presence of anoxemia.The excitability of the auricular muscle was dependent upon the phase of the cardiac cycle (interval from the preceding contraction), and the strength and duration of the square wave stimulus.The length of the absolute refractory period was from 125 to 140 milliseconds, and that of the relative refractory period from 70 to 80 milliseconds, the total refractory period being approximately 10 milliseconds shorter than that of the ventricular muscle.In most cases the threshold of the left auricular muscle was lower than that of the right. The supernormal phase and the dip phenomenon were observed in three cases respectively; however no interrelationship was found between them. It was found that various conditions affected the presence or absence of the supernormal phase.Latent period, i. e., the interval between the delivery of the stimulus and the occurrence of the extrasystolic beat was longer, when the stimulus was given in the initial phase of the cardiac cycle; but it was shortest, when given in or around the dip. In many cases anoxia tended to shorten the latent period. The interval between the preceding auricular wave and the onset of extrasytoric beat, i. e., the coupling time was almost constant, when the stimulus was applied in the initial two thirds of the relative refractory period.In anoxic state, the threshold value of strength of the stimulus increased with an increase in the degree of anoxia. Mild anoxia only slightly affected the refractory period, while severe anoxia prolonged both the absolute and relative refractory period. The conduction velocity within the atria was scarcely affected by mild anoxia but was considerably delayed by severe anoxia. From the above findings, it may be concluded that the excitability of the atria was first accelerated in anoxia then inhibited with the development of more severe anoxia.The vulnerable period was observed in three cases; in one case the fibrillation threshold was lowered by anoxia and the vulnerable period disappeared with inhaltation of pure oxygen but again appeared when pure oxygen was stopped. It may be assumed that atrial fibrillation is more likely to occur in anoxia.From the fact that the latent period was shortened around the dip and that it shortened further in anoxia, it may be possible to infer the presence of a certain relationship between latency and the development of auricular fibrillation, though its true mechanism is not easy to clarify.The artio-ventricular conduction system had a longer refractory period than the proper cardiac muscle and was greatly affected by anoxia.
社団法人日本循環器学会の論文
1959-03-20

犬心房の興奮性に關する實驗的研究

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