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在麻醉条件下,阿托品能在切除肾上腺的大白鼠产生降压作用;但在切除腎上腺的利血平化动物,降压作用反转为升压作用。这种升压作用既不被可卡因所增敏,又不被苄唑啉所拮抗,故与交感机制无关。同时,新斯的明的降压效应又能被利血平化所显著增强。因此认为,在利血平的降压机制中除了目前公认的交感神经功能低落的因素外,尚有副交感神经张力提高的因素参与,而上述条件下阿托品的升压作用乃其抗副交感作用的表现。
Under anesthesia, atropine can produce antihypertensive effect in rats with adrenal removal; but in reserpine-depleted animals that have had adrenal ablation, the antihypertensive effect is reversed. This boost is neither sensitized by cocaine nor antagonized by benzylzoline, so it has nothing to do with the sympathetic mechanism. At the same time, neostigmine’s antihypertensive effect can be markedly enhanced by reserpine. Therefore, in the antihypertensive mechanism of reserpine, in addition to the currently accepted factors of sympathetic dysfunction, there are also factors that contribute to the increase of parasympathetic tone, and the boosting effect of atropine under the above conditions is a manifestation of its anti-parasympathetic effect .