Pfenninger E, Ahnefeld F W, Grünert A
Anaesthesist. 1985 Apr;34(4):191-6.
A sequence of i.v. ketamine injections, 0.5, 2.0, and 5.0 mg/kg body weight, was given to thirty piglets. At the beginning of the investigation, 10 of these animals had a normal intracranial pressure and stable circulation. The intracranial pressure of the remaining 20 piglets was raised to 30 mm Hg, and an additional haemorrhagic shock was induced in 10 of these animals. Those animals with a normal intracranial pressure showed no alteration there of at any of the three doses given, and the arterial pCO2 remained practically unchanged. In contrast, all animals with a raised intracranial pressure, both with and without superimposed haemorrhagic shock, had a significant rise in intracranial pressure and pCO2. These two parameters were found to correlate well with each other. We conclude that in the model used, where the animals were breathing spontaneously, the intracranial pressure rise seen following ketamine application is secondary to the increase in pCO2.
给30只仔猪静脉注射一系列剂量的氯胺酮，分别为0.5、2.0和5.0毫克/千克体重。在研究开始时，其中10只动物颅内压正常且循环稳定。其余20只仔猪的颅内压升高至30毫米汞柱，其中10只动物还诱发了失血性休克。颅内压正常的动物在给予的三个剂量中的任何一个剂量下，颅内压均无变化，动脉血二氧化碳分压（pCO2）实际上也保持不变。相比之下，所有颅内压升高的动物，无论是否叠加失血性休克，颅内压和pCO2均显著升高。发现这两个参数之间具有良好的相关性。我们得出结论，在所使用的模型中，动物为自主呼吸，应用氯胺酮后出现的颅内压升高是继发于pCO2的升高。
