Sonntag H, Stephan H, Lange H, Rieke H, Kettler D, Martschausky N
Department of Anesthesiology, Georg-August-University of Göttingen, West Germany.
Anesth Analg. 1989 May;68(5):584-92.
The effects of a moderate dose of sufentanil (1 microgram.kg-1 + 0.015 micrograms.kg-1.min-1) plus nitrous oxide (30% O2/70% N2O) anesthesia (group I; n = 8) and of high-dose sufentanil/O2 anesthesia (10 micrograms.kg-1 + 0.15 micrograms.kg-1.min-1) without N2O (group II; n = 8) on cardiovascular dynamics, myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, and hypoxanthine release were studied in two groups of male patients scheduled for elective coronary artery bypass surgery. All patients were on maintenance doses of calcium channel blockers and nitrates with the last doses of medications given the morning of operation. All patients were premedicated with flunitrazepam (2 mg orally), piritramide (7.5 mg IM) and promethazine (25 mg IM). Measurements were performed before the induction of anesthesia with the patients premedicated but awake; 20 min after induction of anesthesia with sufentanil plus pancuronium 0.1 mg.kg-1 for muscle relaxation before surgery; and during sternotomy and sternal spread. Sufentanil at either dose decreased mean arterial pressure, as well as cardiac and stroke volume index while heart rate remained unchanged. Following the induction myocardial blood flow and myocardial oxygen consumption decreased 23% (79 ml.min-1.100 g-1 to 61 ml.min-1.100 g-1 and 28% (9.2 ml O2.min-1.100 g-1 to 6.6 ml O2.min-1.100 g-1) in group I and 14% (78 ml.min-1.100 g-1 to 67 ml.min-1.100 g-1 and 18% (8.7 ml O2.min-1.100 g-1 to 7.1 ml O2.min-1.100 g-1) in group II. Myocardial ischemia was seen in one patient of group II (patient No. 4), as indicated by a hypoxanthine release into the coronary sinus, when after the induction MAP decreased from 93 to 67 mm Hg and heart rate increased from 56 to 71 min-1. During sternotomy 8 of 16 patients (50%) developed hypertension and 9 of 16 patients (56%) showed signs of myocardial ischemia, i.e., a lactate and hypoxanthine release.(ABSTRACT TRUNCATED AT 250 WORDS)
在两组计划进行择期冠状动脉搭桥手术的男性患者中，研究了中等剂量舒芬太尼（1微克·千克⁻¹ + 0.015微克·千克⁻¹·分钟⁻¹）加氧化亚氮（30% O₂/70% N₂O）麻醉（I组；n = 8）和高剂量舒芬太尼/O₂麻醉（10微克·千克⁻¹ + 0.15微克·千克⁻¹·分钟⁻¹）且无N₂O（II组；n = 8）对心血管动力学、心肌血流、心肌氧消耗、心肌乳酸平衡和次黄嘌呤释放的影响。所有患者均维持服用钙通道阻滞剂和硝酸盐，最后一剂药物于手术当天上午给药。所有患者均用氟硝西泮（口服2毫克）、匹利卡明（肌内注射7.5毫克）和异丙嗪（肌内注射25毫克）进行术前用药。在患者术前用药但清醒时、用舒芬太尼加泮库溴铵0.1毫克·千克⁻¹诱导麻醉20分钟后（用于术前肌肉松弛）以及胸骨切开术和胸骨撑开期间进行测量。两种剂量的舒芬太尼均降低了平均动脉压以及心脏指数和每搏量指数，而心率保持不变。诱导后，I组心肌血流和心肌氧消耗分别降低了23%（从79毫升·分钟⁻¹·100克⁻¹降至61毫升·分钟⁻¹·100克⁻¹）和28%（从9.2毫升O₂·分钟⁻¹·100克⁻¹降至6.6毫升O₂·分钟⁻¹·100克⁻¹），II组分别降低了14%（从78毫升·分钟⁻¹·100克⁻¹降至67毫升·分钟⁻¹·100克⁻¹）和18%（从8.7毫升O₂·分钟⁻¹·100克⁻¹降至7.1毫升O₂·分钟⁻¹·100克⁻¹）。II组一名患者（4号患者）出现心肌缺血，表现为冠状动脉窦次黄嘌呤释放增加，诱导后平均动脉压从93毫米汞柱降至67毫米汞柱，心率从56次/分钟增至71次/分钟。胸骨切开术期间，16名患者中有8名（50%）出现高血压，16名患者中有9名（56%）出现心肌缺血迹象，即乳酸和次黄嘌呤释放增加。（摘要截断于250字）
