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yi zuo dan zuo he mi zou shen jian dui li ti zuo shu xin fang de xing fen xiao ying
Pages: 8-16
Year: Issue:  1
Journal: Acta Physiologica Sinica

Keyword:  兴奋效应阿托品化蛇根草素心房肾上腺素乙酸心肌胆酸迷走豚鼠;
Abstract: The excitatory action of both vagus stimulation and acetylcholine (ACh) administration on the isolated mammalian heart has been reported by various authors under various experimental conditions, and with various explanations. Thus it has been supposed to be due to liberation of adrenaline-like substance from ganglion cells or chromaffin tissue in the heart; the direct stimulating action of ACh on heart muscle; the restoration of ability of ACh synthesis by heart muscle tissue; etc. The present study deals with the mechanism of action of vagus nerve and ACh on the isolated guinea-pig atria suspened in Locke solution under two different experimental conditions: (1) after atropinization at a bath temperature of 25-30℃; (2) the bath temperature was lowered sufficiently so that spcntaneous rhythmic contractions of the heart was just abolished. In both Cases the excitatory actions of vagus stimulation and ACh administration were easily confirmed. Such action Was abglished by the ganglionic-blocking agent tetraethylammonium (TEA) and nicotine, or by the adrenolytic drugs yohimbine and "Sy-28", whether in the atropinized or in the cooled atrium. After administration of reserpine (5mg/kg) to the animal which deprived the heart tissue of adrenaline-like substance, the excitatory action of ACh on the atrium was abolished. When the dosage of reserpine was increased three-fold, stimulation of vagus also exerted no more excitatory action on the cooled heart. The results of our experiments therefore suggest that the excitatory action of ACh and vagus nerve stimulation on both the atropinized and the cooled atria is associated with the liberation of adrenaline-like substance from the heart tissue. However, we do not think the locus of adreraline liberation is in the ganglion or chromaffine tissue, but instead is in the heart muscle fibre itself, for the excitatory action of ACh is independent of nerve element in the heart, as pointed out by Hsu and Yang previously (1948). If it is assumed that there are two ACh "receptor systems" in the heart muscle, one inhibitory, which is more apt to be paralyzed by atropine and cooling, while the other is excitatory, which is more apt to be paralyzed by "ganglion blocking" drugs, then it may further be assumed that the so-called "excitatory receptor" of the heart muscle is actually a form of boundadrenaline-like substance. The latter, being bound and inactive in heart muscle, is without physiological action, but it can be activated and liberated by the addition of ACh. The reason why it needs a greater dosage of reserpine to discharge the adrenline-like substance which is actived by the vagus is probably because of the situation of the receptor is deeper and less accessible to, the circulating reserpine.
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