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在戊巴比妥钠麻醉兔观察酒石酸锑钾(锑钾)对电致颤阈的影响,锑钾本身所致的心室颤动,以及心脏神经对锑钾作用的影响。结果发现:一定剂量的锑鉮(依次地静脉注射3,6,12毫克/公斤)能显著地降低电致颤阈(9/10兔),并使心率稍有加速(8/10兔),血压缓慢而逐步下降;大剂量(24—36毫克/公斤)使血压迅速而显著下降,6/10兔出现锑致性心室颤动。在切断迷走神经,切除交感神经或利血平化以后,锑钾的降低电致颤阈的作用不仅被防止并且全部翻轉,阿托品(0.2或2毫克/公斤)均不能显著地影响这种致颤阈的降低。锑钾所致的心率加速作用为切除交感神经,利血平化或大剂量阿托品所防止而且翻轉,相反,在切断迷走神经与小剂量阿托品后,心率加速仍然出现。切断迷走神经与小剂量阿托品完全不能防止锑致性心室颤动,分别仍有4/5与5/6兔出现颤动,而切除交感神经,利血平化或大剂量阿托品则能完全防止之。此外,于不麻醉兔小剂量阿托品不影响,而大剂量阿托品能防止去甲腎上腺素的心律紊乱。根据实验结果,可以作出推论如下:在本实验条件下锑钾的降低电致颤阈的作用是与心脏交感神经的完整性或心内儿茶酚胺储存量有关;至于迷走神经的意义尚待阐明,可能为组成此反射弧的传入通路,而以交感神经为其传出通路。锑钾加速心率的作用及大剂量所致的锑致性心室颤动则与迷走神经无关,而是取决于交感神经的完整性或心肌内的儿茶酚胺储存量。大剂量阿托品对锑致性心室颤动与去甲腎上腺素的心律紊乱均有保护作用,这可能是通过对抗迷走神经以外的机制。
The effects of antimony potassium tartrate (antimony potassium) on the threshold of electrical shock, ventricular fibrillation induced by antimony potassium itself, and the effects of cardiac nerves on antimony potassium were observed in sodium pentobarbital anesthetized rabbits. The results showed that a dose of antimony tartrate (3, 6, 12 mg / kg iv) was able to significantly reduce the electrflexance threshold (9/10 rabbits) and slightly accelerate the heart rate (8/10 rabbits) Slow and gradual decrease in blood pressure; high dose (24-36 mg / kg) to make rapid and significant drop in blood pressure, anti rabbit induced anti-ventricular fibrillation in 6/10. After cutting off the vagus nerve, resecting sympathetic or reserpine, the action of antimony trispermine to reduce the electrical tremor threshold was not only prevented but also completely reversed, and neither atropine (0.2 or 2 mg / kg) significantly affected this threshold The reduction. Antimony potassium accelerated heart rate due to resection of sympathetic, reserpine or high-dose atropine to prevent and flip, on the contrary, after cutting off the vagus nerve and low-dose atropine, the heart rate still occur. Cut off the vagus nerve and small doses of atropine can not prevent antimony-induced ventricular fibrillation, respectively, there are still 4/5 and 5/6 rabbits appear fibrillation, and removal of sympathetic, reserpine or high-dose atropine can completely prevent it. In addition, small doses of atropine do not anesthetize rabbit does not affect the high dose of atropine to prevent norepinephrine heart rhythm disorders. According to the experimental results, the following conclusions can be drawn: The anti-fibrillation threshold of antimony potassium under this experimental condition is related to the integrity of cardiac sympathetic nerve or the storage of cardiac catecholamine. The significance of vagal nerve needs to be elucidated Composition of this reflection arc of the incoming pathways, and the sympathetic to its outgoing path. Antimony potassium to accelerate the role of heart rate and high doses of antimony-induced ventricular fibrillation and the vagus nerve has nothing to do, but depends on the integrity of the sympathetic or myocardial catecholamine storage. High-dose atropine has protective effects on antimony-induced ventricular fibrillation and norepinephrine arrhythmias, which may be through mechanisms other than antagonizing the vagus nerve.