Singbartl G, Langrehr D, Neuhaus R
Prakt Anaesth. 1975 Dec;10(6):335-44.
Induction anaesthesia with 2 mg/kg of ketamine causes the well-known increases in heart rate and blood pressure. Simultaneous registration of the systolic-time-intervals (PEPI, LVETTI, PEP/LVET = Q), however, reveals a biphasic effect of ketamine on these contractility-parameters: an initial increase of PEPI and Q, representing a cardiac depressive effect of ketamine, is followed by a decrease of PEPI and Q, indicating a positive inotropic action of ketamine. Injecting the same dose of ketamine during the steady-state of a halothane-N2O:O2-anaesthesia, that causes a depression of the central and peripheral sympathetic activity, however, results in an increase of PEPI and Q, only. Thus, ketamine is a cardiac depressive agent, this effect, however, usually being overlapped by a centrally-induced cardiac stimulation.
2毫克/千克的氯胺酮诱导麻醉会导致心率和血压出现众所周知的升高。然而，同时记录收缩期时间间隔（PEPI、LVETTI、PEP/LVET = Q）显示氯胺酮对这些收缩性参数有双相作用：PEPI和Q最初升高，代表氯胺酮的心脏抑制作用，随后PEPI和Q降低，表明氯胺酮有正性肌力作用。然而，在氟烷-N₂O:O₂麻醉的稳态期间注射相同剂量的氯胺酮，这会导致中枢和外周交感神经活动受到抑制，结果仅导致PEPI和Q升高。因此，氯胺酮是一种心脏抑制药物，不过这种作用通常会被中枢诱导的心脏刺激所掩盖。
