Pfenninger E, Grünert A, Bowdler I, Kilian J
Acta Neurochir (Wien). 1985;78(3-4):113-8. doi: 10.1007/BF01808689.
Seventeen piglets of both sexes, seven with O2/air-buprenorphine anaesthesia and controlled ventilation, and ten unanaesthetized animals with normal, spontaneous respiration, were used for the study. The intracranial pressure of both groups of animals was raised by insufflation of an epidural balloon and the arterial blood pressure was reduced to approximately 70% of the original value by controlled haemorrhage. 0.5 mg/kg body weight of ketamine was given intravenously, followed by a further dose of 2.0 mg/kg body weight of ketamine five minutes later. Both ketamine doses led to a significant rise in the intracranial pressure of those animals breathing spontaneously (31.8 mm Hg to 39.1 mm Hg). In contrast, the ventilated animals showed a significant reduction in intracranial pressure. No changes in arterial PCO2 were observed in this group, while those piglets breathing spontaneously had dangerous PCO2 rises. At both ketamine doses a significant correlation could be found between the PCO2 and the intracranial pressure.
选用17只仔猪，其中7只用氧气/空气-丁丙诺啡麻醉并控制通气，10只未麻醉、有正常自主呼吸的动物用于该研究。两组动物均通过硬膜外球囊充气使颅内压升高，并通过控制性出血使动脉血压降至原始值的约70%。静脉注射0.5mg/kg体重的氯胺酮，5分钟后再注射2.0mg/kg体重的氯胺酮。两次氯胺酮给药均导致自主呼吸动物的颅内压显著升高（从31.8mmHg升至39.1mmHg）。相比之下，通气动物的颅内压显著降低。该组未观察到动脉PCO₂变化，而自主呼吸的仔猪出现危险的PCO₂升高。在两个氯胺酮剂量下，PCO₂与颅内压之间均存在显著相关性。
