Filippelli A, Cuparencu B, Falciani M, de Novellis V, Safta L, Arustei V, Rossi F
Institute of Pharmacology and Toxicology, Faculty of Medicine and Surgery II, University of Naples, Italy.
Res Commun Chem Pathol Pharmacol. 1994 Jun;84(3):331-40.
In urethane anesthetized rats the icv (lateral cerebral ventricle) administration of ketamine, at the highest utilized doses, induced bradypnea and sinus bradycardia in spontaneously breathing rats. Moreover, it partially antagonized the arrhythmogenic activities of sodium glutamate and sodium aspartate, as well as desipramine and ouabain. From these results, we conclude that ketamine had an inhibitory effect on the centrogenic arrhythmias not only acting at the level of NMDA subtype receptor, but also at beta 1 adrenergic central receptors. Moreover at high doses, ketamine can also induce centrogenic arrhythmias in spontaneously breathing rats.
在氨基甲酸乙酯麻醉的大鼠中，向侧脑室注射氯胺酮，在使用的最高剂量下，会导致自主呼吸的大鼠出现呼吸过缓和窦性心动过缓。此外，它部分拮抗了谷氨酸钠、天冬氨酸钠以及地昔帕明和哇巴因的致心律失常活性。从这些结果来看，我们得出结论，氯胺酮不仅在N-甲基-D-天冬氨酸（NMDA）亚型受体水平，而且在β1肾上腺素能中枢受体水平，对中枢性心律失常都有抑制作用。此外，高剂量时，氯胺酮也可在自主呼吸的大鼠中诱发中枢性心律失常。
