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前文报导,在麻醉兎观察酒石酸銻鉀(簡称銻鉀)对电致心室顫动的影响实驗中,发現在实驗后期,大剂量銻鉀本身也能产生心室顫动,而这种銻致性心室顫动能被預先切断交感神經或利血平化所防止。本文采用与前文相同的实驗模型和条件,对家兎心室內儿茶酚胺含量进行了生物测定。发現盐水对照组心室儿茶酚胺含量平均为1.13±0.06微克/克。电刺激对照組为1.72±0.45,虽与盐水对照组相比在統計学上差別不显著,但波动較大。在电刺激加銻鉀组中,銻鉀能显著降低全部动物的电致顫阈,稍加速心率,并使6/11兎出現銻致性心室顫动,心室儿茶酚胺含显著减少至0.65±0.05。单注射銻钾組心肌儿茶酚胺含量平均为0.47±0.08,較盐水对照組显著减少,但与电刺激加銻鉀组差別不显著。利血平化(0.1毫克/公斤/天,共2次)后,兎心儿茶酚胺充份地被耗竭,含量降至0.032±0.003,耗竭程度达97％。利血平化后电刺激加銻鉀组的心室儿茶酚胺含量为0.041±0.010,銻致性心室顫动并不出現。上述資料对前文的推論提出直接証明,卽儿茶酚胺在該种心律紊乱发病机制中具有重要意义。除儿茶酚胺含量外,我們又进行了心室乙酰胆碱含量的测定,发現正常盐水对照家兎心室乙酰胆碱含量平均为0.323±0.013微克/克。銻鉀一次大剂量注射或銻鉀三日給药法均不明显改变其含量。預先切断迷走神經或注射大剂量阿托品后再給大剂量銻鉀,也对心室乙酰胆碱含量无明显影响。因此完全不能証实黄铭新等关于这方面的报导。利血平在对家兎銻致性顫动具有防止作用的剂量下并不影响心室乙酰胆碱含量,較大剂量却能显著提高豚鼠心室乙酰胆碱的含量(P<0.01)。这些資料也完全支持前文所作出的推論,卽迷走神經在这种实驗性心律紊乱发病机制中的意义不大。
Previously reported in anesthesia 兎 observed antimony tartrate potassium (antimony potassium) on the impact of electrical shock on ventricular fibrillation in the experiment found that high doses of antimony potassium itself can produce ventricular fibrillation, and this antimony-induced Ventricular fibrillation can be prevented by pre-cutting sympathetic or reserpine levels. In this paper, the same experimental model and conditions as above were used to determine the bioavailability of catecholamines in the plasma of the housefly. The mean cortisol levels in the saline control group were found to be 1.13 ± 0.06 μg / g. The electrical stimulation control group was 1.72 ± 0.45, although the difference was not statistically significant compared with the saline control group, but the fluctuation was larger. Antimony potassium increased electrical shock threshold, slightly accelerated heart rate and antimony-induced ventricular fibrillation in 6/11, group, while ventricular catecholamine significantly decreased to 0.65 ± 0.05 in anti-stibium group. The average myocardial catecholamines concentration in antimony mono-potassium group was 0.47 ± 0.08, which was significantly lower than that in saline control group, but not significantly different from that in antimony-stimulated potassium group. After reserpine (0.1 mg / kg / day for 2 times), catecholamine was exhausted to a level of 0.032 ± 0.003 with a depletion of 97%. The level of ventricular catecholamines in reserpine-treated and antimony-stimulated groups was 0.041 ± 0.010, and antimony-induced ventricular fibrillation did not occur. The above information provides a direct proof of the above corollary, catecholamines in the pathogenesis of heart rhythm is of great significance. In addition to catecholamine levels, we performed a ventricular acetylcholine assay and found that the average acetylcholine concentration in normal saline control housefly was 0.323 ± 0.013 μg / g. A large dose of antimony potassium injection or antimony potassium three days administration were not significantly changed its content. Pre-cut off the vagus nerve or injection of large doses of atropine and then give high-dose antimony potassium, but also on the ventricular acetylcholine content had no significant effect. So can not confirm Huang Mingxin and other reports on this area. Reserpine did not affect the content of acetylcholine in the ventricular with the dose of antimony-induced tremor, and the higher dose could significantly increase the content of acetylcholine in guinea pig ventricular (P <0.01). These data also fully support the previous inference, 卽 vagus nerve in the pathogenesis of experimental heart rhythm is of little significance.