Sheehan P B, Zornow M H, Scheller M S, Peterson B M
Division of Pediatric Critical Care, Children's Hospital and Health Center, San Diego, La Jolla, California, USA.
J Neurosurg Anesthesiol. 1992 Oct;4(4):261-7. doi: 10.1097/00008506-199210000-00006.
The cerebrovascular response to the administration of equipotent doses of fentanyl and sufentanil was evaluated in New Zealand white rabbits following cryogenic brain injury. In a preliminary study consisting of 10 animals, it was documented that the cerebral blood flow response to alterations in the PaCO2 remained intact in this model of brain injury. Subsequently, 28 rabbits were anesthetized with 1.5% halothane in oxygen, paralyzed with pancuronium, and mechanically ventilated. A cryogenic lesion was created over the left hemisphere. One hour later, the intracranial pressure had risen to a mean value of 15 mm Hg. Baseline measurements were then made of monitored variables, which included heart rate, mean arterial pressure, central venous pressure, intracranial pressure, temperature, and arterial blood gases. Global cerebral blood flow was measured utilizing a hydrogen clearance technique. The animals were then randomized to receive an infusion of fentanyl (N = 9, 200 microg/kg), sufentanil (N = 10, 20 microg/kg), or an equal volume of normal saline (N = 9) by i.v. infusion over 5 min. At the conclusion of the opioid infusions, repeated measurements of hemodynamic variables and intracranial pressure were recorded for 15 min and a second cerebral blood flow measurement was made. There were no significant differences in mean arterial pressure, heart rate, central venous pressure, intracranial pressure, cerebral blood flow, or blood gas values between the three groups prior to the administration of fentanyl, sufentanil, or normal saline. At the conclusion of the 5 min infusion, the intracranial pressure had increased by approximately 5 mm Hg in all three groups. The mean arterial pressure decreased to a similar degree in the fentanyl and sufentanil groups and was significantly lower than the mean arterial pressure in the saline group. Although the cerebral perfusion pressure decreased in all three groups, cerebral blood flow was not significantly affected. These results suggest that there is no significant difference in the effects of fentanyl vs. sufentanil on mean arterial pressure, intracranial pressure, or cerebral blood flow in this model of acute brain injury and elevated intracranial pressure.
在新西兰白兔发生低温性脑损伤后，评估了等效剂量芬太尼和舒芬太尼给药后的脑血管反应。在一项由10只动物组成的初步研究中，记录到在该脑损伤模型中，脑血流对动脉血二氧化碳分压变化的反应保持完好。随后，28只兔子用1.5%的氟烷加氧气麻醉，用泮库溴铵使其麻痹，并进行机械通气。在左半球制造一个低温损伤。1小时后，颅内压升至平均15毫米汞柱。然后对监测变量进行基线测量，这些变量包括心率、平均动脉压、中心静脉压、颅内压、体温和动脉血气。利用氢清除技术测量全脑血流量。然后将动物随机分为静脉输注芬太尼（N = 9，200微克/千克）、舒芬太尼（N = 10，20微克/千克）或等体积生理盐水（N = 9）组，在5分钟内静脉输注。在阿片类药物输注结束时，记录15分钟内血流动力学变量和颅内压的重复测量值，并进行第二次脑血流量测量。在给予芬太尼、舒芬太尼或生理盐水之前，三组之间的平均动脉压、心率、中心静脉压、颅内压、脑血流量或血气值没有显著差异。在5分钟输注结束时，三组的颅内压均升高了约5毫米汞柱。芬太尼组和舒芬太尼组的平均动脉压下降程度相似，且显著低于生理盐水组的平均动脉压。尽管三组的脑灌注压均下降，但脑血流量未受到显著影响。这些结果表明，在该急性脑损伤和颅内压升高模型中，芬太尼与舒芬太尼对平均动脉压、颅内压或脑血流量的影响没有显著差异。
