Matsumura C, Kemmotsu O, Kawano Y, Takita K, Sugimoto H, Mayumi T
Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, Sapporo, Japan.
J Clin Anesth. 1994 Sep-Oct;6(5):419-24. doi: 10.1016/s0952-8180(05)80015-7.
To determine whether serum and urine inorganic fluoride levels with prolonged (more than 7 hours) low-dose (0.8 to 2.0 vol %) sevoflurane anesthesia plus epidural anesthesia were increased as compared with isoflurane anesthesia plus epidural anesthesia. To measure the urine tubular enzymes N-acetyl-beta-glucosaminidase (NAG), alpha 1-microglobulin (alpha 1-M), and beta 2-microglobulin (beta 2-M) for renal tubular injury in both groups.
Randomized, prospective study.
University hospital.
15 ASA physical status I and II adults (7 males, 8 females) who were scheduled for prolonged laparotomy (lasting 9.5 to 10.2 hours) with general anesthesia.
Epidural anesthesia was administered before induction of general anesthesia. General anesthesia was induced with thiamylal administered intravenously (IV), and the trachea was intubated following administration of vecuronium IV. It was maintained with either sevoflurane or isoflurane in nitrous oxide and oxygen. Standard monitoring was used in all patients. Serum and urine inorganic fluoride and urine tubular enzymes were measured periodically. Serum inorganic fluoride was 54 mumol/L at 4.3 minimum alveolar concentration (MAC) hours of sevoflurane; the peak level for isoflurane was 8 mumol/L at the same MAC hours. Sevoflurane also increased urine inorganic fluoride excretion to 96 mumol/hr 8 hours. NAG excretion started to increase after inhalation of either sevoflurane or isoflurane. alpha 1-M and beta 2-M excretion increased markedly postoperatively. Even though fluoride levels and tubular enzymes were high, there was no evidence of postoperative renal dysfunction.
There was no increase in urinary enzymes, which are indicators of tubular injury, specific to sevoflurane. There was no postoperative renal dysfunction, as indicated by unchanged serum creatinine and blood urea nitrogen levels.
确定与异氟烷麻醉加硬膜外麻醉相比,长时间(超过7小时)低剂量(0.8%至2.0%体积分数)七氟烷麻醉加硬膜外麻醉时血清和尿液无机氟水平是否升高。测量两组患者肾小管损伤的尿肾小管酶N - 乙酰 - β - 氨基葡萄糖苷酶(NAG)、α1 - 微球蛋白(α1 - M)和β2 - 微球蛋白(β2 - M)。
随机前瞻性研究。
大学医院。
15例ASA身体状况为I级和II级的成人(7例男性,8例女性),计划接受全身麻醉下的长时间剖腹手术(持续9.5至10.2小时)。
在全身麻醉诱导前给予硬膜外麻醉。全身麻醉诱导采用静脉注射硫喷妥钠,静脉注射维库溴铵后进行气管插管。用七氟烷或异氟烷加氧化亚氮和氧气维持麻醉。所有患者均采用标准监测。定期测量血清和尿液无机氟及尿肾小管酶。七氟烷在4.3倍最低肺泡浓度(MAC)小时时血清无机氟为54μmol/L;异氟烷在相同MAC小时时的峰值水平为8μmol/L。七氟烷还使8小时时尿无机氟排泄增加至96μmol/小时。吸入七氟烷或异氟烷后NAG排泄开始增加。术后α1 - M和β2 - M排泄明显增加。尽管氟水平和肾小管酶升高,但没有术后肾功能障碍的证据。
作为肾小管损伤指标的尿酶没有因七氟烷而特异性增加。血清肌酐和血尿素氮水平未改变,表明没有术后肾功能障碍。