论文部分内容阅读
我们曾用阿托品有效地预防用电刺激下丘脑和静脉注射儿茶酚胺及用毒毛旋花子甙——K诱发兔的心律失常。本实验是在由毒毛旋花子甙——K(下称毒——K)诱发兔心律失常的基础上,进一步观察迷走神经的作用。实验结果表明:在迷走神经完整时,静注毒——K加阿托品(剂量均为0.3 mg/kg)可以显示出阿托品的预防效果;而切断双侧迷走神经后注射同量毒——K加阿托品,则几乎所有实验兔均发生严常心律失常(室颤),表明保持迷走神经完整具有重要意义。交感神经亢进在心律失常的发病中的重要作用,已较肯定,而关于迷走神经所起的作用,则有争论。毛地黄类中毒所致的心律失常神经因素中,中毒剂量毛地黄引起交感神经亢进,促进异搏点自律性增高或折返机制的形成,已为多数学者公认。毛地黄中毒引起的窦性心动过缓,房室传导阻滞,被认为是由于迷走神经亢进所致Gillis等人认为中毒剂量毛地黄可同时激发交感和副交神经活动的亢进。我们曾用阿托品有效地预防用电刺激下丘脑和静脉注射儿茶酚胺及用中毒剂量毒——K诱发兔的心律失常,并提出阿托品对心律失常的预防作用可能与迷走神经有关的推想。本实验是在由毒——K诱发兔心律失常的实验基础上,进一步观察迷走神经的作用。为探讨此类心律失常发生的神经机制,提供参考资料。
We have used atropine to effectively prevent electrical stimulation of catecholamines in the hypothalamus and vein and the induction of arrhythmia in rabbits by venom-kappa-cyclase. This experiment is to further observe the role of vagus nerve on the basis of venom arrhythmia induced by venom of spinosad - K (hereinafter referred to as poison - K). The experimental results show that: in the vagus nerve integrity, intravenous injection of poison - K plus atropine (both doses of 0.3 mg / kg) can show the prophylactic effect of atropine; while the bilateral vagus nerve is cut off after injection of the same amount of poison - K plus atropine, Almost all experimental rabbits had atrial arrhythmia (VF), indicating that maintaining the integrity of the vagus nerve is of great importance. The important role of sympathetic hyperactivity in the pathogenesis of arrhythmia has been more certain, and the role of the vagus nerve has been debated. Foxpox poisoning caused by arrhythmic neurological factors, poisoning dose of yellow caused by sympathetic hyperthyroidism, to promote the heterotaxis point of self-discipline or the formation of the mechanism of reentry, has been recognized by most scholars. Sinus bradycardia caused by sinus bradycardia, atrioventricular block, is believed to be due to vagal hyperactivity caused by Gillis and others that the toxic dose of digitalis can stimulate sympathetic and parasympathetic activity hyperthyroidism. We have used atropine to effectively prevent electrical stimulation of catecholamines in the hypothalamus and vein and toxic arrhythmia in rabbits with toxic doses of kappa-K and suggest that the prophylaxis of arrhythmia by atropine may be related to the vagus nerve. This experiment is based on the experiment of poison-K-induced arrhythmia in rabbits to further observe the role of the vagus nerve. In order to explore the neural mechanism of such arrhythmia, provide reference materials.