Nakajima T, Azumi T, Iwasaki H, Kaneshiro S, Yatabe Y
Arch Int Pharmacodyn Ther. 1977 Jul;228(1):108-17.
Effect of ketamine on the SA node of the dog heart was studied in vivo using a selective perfusion technique of the SA node artery. Injections of ketamine in doses from 100 microgram to 3 mg into the artery produced a depression of the SA nodal activity by a direct action. This depression was followed by the sudden appearance of a stimulatory phase. Bilateral vagotomy and sympathectomy or prior administration of a ganglion blocker failed to inhibit the occurrence of the ketamine-induced tachycardia, while it was completely abolished in the reserpinized dogs or by a prior injection of a beta-blocking agent into the SA node artery. This may indicate that an activation of the peripheral adrenergic mechanism plays an important role in the induction of the excitatory effect of ketamine injected in the SA node artery.
采用窦房结动脉选择性灌注技术,在体研究了氯胺酮对犬心脏窦房结的作用。向动脉内注射100微克至3毫克剂量的氯胺酮,可通过直接作用抑制窦房结活动。这种抑制之后会突然出现兴奋期。双侧迷走神经切断术和交感神经切除术或预先给予神经节阻滞剂均未能抑制氯胺酮诱导的心动过速的发生,而在利血平化的犬中或预先向窦房结动脉注射β受体阻滞剂后,心动过速则完全消失。这可能表明,外周肾上腺素能机制的激活在窦房结动脉注射氯胺酮所诱导的兴奋效应中起重要作用。