Piepenbrock S, Zenz M, Reichelt W, Wölfel D, Reinhart K
Anaesthesist. 1983 Feb;32(2):67-74.
In 10 healthy patients, buprenorphine was given as the postoperative analgesic (dosage: peripheral venous injection of 5 microgram/kg BW) after traumatological interventions in the lower extremities, which had been performed under barbiturate-induced halothane anaesthesia. The haemodynamic investigations revealed that buprenorphine has only a minor effect on the high pressure system. In the area of the pulmonary circulation, there was a significant increase in mean pulmonary artery pressure from 15.9 mm Hg to 17.8 mm Hg (+12%), as well as an increase in pulmonary vascular resistance by 16.5%. These changes were most marked 30 to 60 min after the administration of buprenorphine. When 2-3 1 O2/min were administered, none of the patients had PaO2 values of less than 100 mm Hg. 60 min after the injection, the PaCO2 value increased from 33.7 mm Hg to a maximum of 43.9 mm Hg. In 3 patients, PaCO2 increased to more than 45 mm Hg. All patients with greater increases of PaCO2 also evidenced greater increases in the pulmonary vascular resistance. Altogether the haemodynamic changes after buprenorphine administration following halothane anesthesia were not very distinct. In individual cases, however, there were greater increases in PaCO2. The cause of this could involve the additive effects of premedication and anaesthesia medication, and possibly the pain level as well. Both the increase in pulmonary artery pressure and the increase in total pulmonary vascular resistance in these patients were due to hypercapnia (von Euler-Liljestrand mechanism).
在10名健康患者中,下肢创伤干预后(手术在巴比妥诱导的氟烷麻醉下进行),给予丁丙诺啡作为术后镇痛药(剂量:外周静脉注射5微克/千克体重)。血流动力学研究表明,丁丙诺啡对高压系统的影响较小。在肺循环方面,平均肺动脉压从15.9毫米汞柱显著升至17.8毫米汞柱(+12%),肺血管阻力增加16.5%。这些变化在给予丁丙诺啡后30至60分钟最为明显。当以每分钟2 - 3升的速度给予氧气时,没有患者的动脉血氧分压值低于100毫米汞柱。注射后60分钟,动脉血二氧化碳分压值从33.7毫米汞柱升至最高43.9毫米汞柱。3名患者的动脉血二氧化碳分压升至45毫米汞柱以上。所有动脉血二氧化碳分压升高幅度较大的患者,其肺血管阻力也有更大幅度的升高。总体而言,氟烷麻醉后给予丁丙诺啡后的血流动力学变化不太明显。然而,在个别情况下,动脉血二氧化碳分压有较大升高。其原因可能涉及术前用药和麻醉药物的叠加作用,也可能与疼痛程度有关。这些患者肺动脉压升高和总肺血管阻力增加均归因于高碳酸血症(冯·欧拉 - 利耶斯特兰德机制)。