Kanaya Noriaki, Satoh Hitoshi, Seki Sumihiko, Nakayama Masayasu, Namiki Akiyoshi
Department of Anesthesiology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Anesth Analg. 2002 May;94(5):1207-11, table of contents. doi: 10.1097/00000539-200205000-00029.
The induction of anesthesia with propofol is often associated with a decrease in arterial blood pressure (BP). Although vasopressors are sometimes required to reverse the propofol-induced hypotension, little is known about the effect of propofol on these drugs. We studied the effects of propofol and sevoflurane on pressor response to i.v. ephedrine. Thirty adult patients were randomly assigned to one of two groups. In the Propofol group (n = 15), patients received propofol 2.5 mg/kg i.v. for induction followed by 100 microg x kg(-1) x min(-1) i.v. for maintenance. In the Sevoflurane group (n = 15), anesthesia was induced with sevoflurane 3%-4% in oxygen and maintained with sevoflurane 2% in oxygen. All patients in both groups received ephedrine 0.1 mg/kg i.v. before and after the anesthetic induction. Ephedrine increased the heart rate significantly (P < 0.05) in awake patients in both study groups. In contrast, there was no increase in heart rate after the ephedrine administration under propofol or sevoflurane anesthesia. In awake patients, transient increases in mean BP were observed after i.v. ephedrine in both groups. In the Propofol group, 2 min after the administration of ephedrine, mean BP increased 16% +/- 10% under anesthesia but increased only 4% +/- 6% when the same patients were awake. The magnitudes of the pressor responses to ephedrine during propofol anesthesia were significantly greater (P < 0.05) than during the awake state. However, ephedrine 0.1 mg/kg i.v. showed no significant increases in BP during sevoflurane anesthesia. We conclude that propofol, not sevoflurane, anesthesia augments the pressor responses to i.v. ephedrine.
The effect of anesthetics on vasopressor-mediated cardiovascular effects is poorly understood. We evaluated the pressor response to ephedrine during propofol or sevoflurane anesthesia. Our study suggests that anesthesia-induced hypotension may be easier to reverse with ephedrine during propofol anesthesia than during sevoflurane anesthesia.
丙泊酚诱导麻醉常伴有动脉血压(BP)下降。尽管有时需要使用血管升压药来逆转丙泊酚引起的低血压,但丙泊酚对这些药物的影响知之甚少。我们研究了丙泊酚和七氟醚对静脉注射麻黄碱升压反应的影响。30例成年患者随机分为两组。丙泊酚组(n = 15),患者静脉注射丙泊酚2.5 mg/kg诱导麻醉,随后以100 μg·kg⁻¹·min⁻¹静脉维持。七氟醚组(n = 15),用3% - 4%七氟醚与氧气混合诱导麻醉,并用2%七氟醚与氧气混合维持麻醉。两组所有患者在麻醉诱导前后均静脉注射麻黄碱0.1 mg/kg。麻黄碱使两个研究组清醒患者的心率显著增加(P < 0.05)。相比之下,在丙泊酚或七氟醚麻醉下给予麻黄碱后心率没有增加。在清醒患者中,两组静脉注射麻黄碱后平均血压均出现短暂升高。在丙泊酚组,给予麻黄碱2分钟后,麻醉状态下平均血压升高16%±10%,但同一患者清醒时仅升高4%±6%。丙泊酚麻醉期间对麻黄碱的升压反应幅度显著大于清醒状态(P < 0.05)。然而,静脉注射0.1 mg/kg麻黄碱在七氟醚麻醉期间血压无显著升高。我们得出结论,丙泊酚麻醉而非七氟醚麻醉增强了对静脉注射麻黄碱的升压反应。
麻醉药对血管升压药介导的心血管效应的影响了解甚少。我们评估了丙泊酚或七氟醚麻醉期间对麻黄碱的升压反应。我们的研究表明,与七氟醚麻醉相比,丙泊酚麻醉期间麻醉诱导的低血压可能更容易用麻黄碱逆转。