七氟醚在不同气体流量下产生A物质浓度差异及对患者肝肾功能影响
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摘要
背景:七氟醚是世界范围内广泛使用的吸入性麻醉气体,具有众多的临床优点。但是七氟醚和CO_2吸附剂会发生反应,并生成A物质(CA)。CA对小鼠具有肾脏毒性。七氟醚产生CA量的多少取决于CO_2吸附剂中含有的强碱以及水分的多少,以及所使用的气体流量和麻醉仪器。该研究的目的是为了验证在协和医院麻醉科的常规设定下,当患者接受相同浓度和时间的七氟醚暴露时,低气体流量(500ml/min)和高气体流量(2L/min)产生的CA浓度差异,以及患者术前-术后肝肾功能的变化情况。
方法:选择接受普通外科手术的患者(n=16),随机分为高流量组和低流量组。在手术过程中维持患者血压水平稳定(±20%)以及潮气末CO_2浓度,并且根据需要使用镇痛药物。麻醉开始后,每隔30分钟在呼吸管路的吸气端取样,检测CA浓度,同时记录患者的SEV浓度。分别在术前、术后检测患者的肝肾功能(ALT、AST、Tbil、Dbil、BUN、Cr)。
结果:两组患者的SEV浓度(0.9692vs0.9675MAC)以及浓度-时间之间(2.40vs2.41MAC-h)不存在显著差异(p＞0.05)。但是两组的CA浓度(27.70vs11.54ppm)和曲线下面积(AUC)之间(55.76vs23.19ppm-h)存在显著差异。两组患者术前、术后的肝肾功能指标(ALT、AST、Tbil、Dbil、BUN、Cr)无显著改变。
结论:低流量(500ml)和高流量(2L/min)条件下吸入SEV所产生的CA浓度存在显著差异,但是并不会引起患者术前、术后肝肾功能指标的改变,包括ALT、AST、Tbil、Dbil、BUN、Cr。
Background:Sevoflurane is the most popular anesthetic gas in the world,it exhibits many clinical advantages.But sevoflurane is degraded by CO_2 absorbents to Compound A(CA)。CA is known to be nephrotoxic in rats。The amount of CA depends on the strong base and water contents of the carbon dioxide absorbent used,as well as the flow rate and anesthetic machine。The purpose of this study was to measure the amounts of CA produced under the routine circumstances of department of anesthesiology in PUMCH, compare CA concentrations between low-flow anesthesia(500ml) and high-flow anesthesia(2L/min),and the changes of markers of renal and liver injury or dysfunction。
Methods:the general surgical patients(n=16) were randomized to low-flow anesthesia group and high-flow anesthesia group。Maintain the blood pressure(baseline±20%) and the end-tidal CO_2,use analgesic as needed。Gas samples were taken from the inspiratory limbs of the anesthetic circuit in 30-minites interval during anesthesia。Record the SEV concentration。Analyze the markers of renal and liver injury or dysfunctions pre-and post-surgery。
Results:there were no statistical differences(p＞0.05) between SEV concentration (0.9692vs0.9675MAC) and concentration-time(2.40vs2.41MAC-h)。there were significant differences(P＜0.01) between CA concentrations(27.70vs11.54ppm) and AUC(55.76vs23.19ppm-h)。all markers of hepatic and renal function(ALT、AST、Tbil、Dbil、BUN、Cr) were unchanged after anesthesia。
Conclusion:CA concentrations between low-flow(500ml) and high-flow(2L/min) anesthesia were significantly different,but it did not result in any significant change to markers of hepatic and renal function,including ALT、AST、Tbil、Dbil、BUN、Cr。
方法:选择接受普通外科手术的患者(n=16),随机分为高流量组和低流量组。在手术过程中维持患者血压水平稳定(±20%)以及潮气末CO_2浓度,并且根据需要使用镇痛药物。麻醉开始后,每隔30分钟在呼吸管路的吸气端取样,检测CA浓度,同时记录患者的SEV浓度。分别在术前、术后检测患者的肝肾功能(ALT、AST、Tbil、Dbil、BUN、Cr)。
结果:两组患者的SEV浓度(0.9692vs0.9675MAC)以及浓度-时间之间(2.40vs2.41MAC-h)不存在显著差异(p＞0.05)。但是两组的CA浓度(27.70vs11.54ppm)和曲线下面积(AUC)之间(55.76vs23.19ppm-h)存在显著差异。两组患者术前、术后的肝肾功能指标(ALT、AST、Tbil、Dbil、BUN、Cr)无显著改变。
结论:低流量(500ml)和高流量(2L/min)条件下吸入SEV所产生的CA浓度存在显著差异,但是并不会引起患者术前、术后肝肾功能指标的改变,包括ALT、AST、Tbil、Dbil、BUN、Cr。
Background:Sevoflurane is the most popular anesthetic gas in the world,it exhibits many clinical advantages.But sevoflurane is degraded by CO_2 absorbents to Compound A(CA)。CA is known to be nephrotoxic in rats。The amount of CA depends on the strong base and water contents of the carbon dioxide absorbent used,as well as the flow rate and anesthetic machine。The purpose of this study was to measure the amounts of CA produced under the routine circumstances of department of anesthesiology in PUMCH, compare CA concentrations between low-flow anesthesia(500ml) and high-flow anesthesia(2L/min),and the changes of markers of renal and liver injury or dysfunction。
Methods:the general surgical patients(n=16) were randomized to low-flow anesthesia group and high-flow anesthesia group。Maintain the blood pressure(baseline±20%) and the end-tidal CO_2,use analgesic as needed。Gas samples were taken from the inspiratory limbs of the anesthetic circuit in 30-minites interval during anesthesia。Record the SEV concentration。Analyze the markers of renal and liver injury or dysfunctions pre-and post-surgery。
Results:there were no statistical differences(p＞0.05) between SEV concentration (0.9692vs0.9675MAC) and concentration-time(2.40vs2.41MAC-h)。there were significant differences(P＜0.01) between CA concentrations(27.70vs11.54ppm) and AUC(55.76vs23.19ppm-h)。all markers of hepatic and renal function(ALT、AST、Tbil、Dbil、BUN、Cr) were unchanged after anesthesia。
Conclusion:CA concentrations between low-flow(500ml) and high-flow(2L/min) anesthesia were significantly different,but it did not result in any significant change to markers of hepatic and renal function,including ALT、AST、Tbil、Dbil、BUN、Cr。
引文
1. Wallin R, Regan B, Napoli M, Stern I. Sevoflurane: a new inhalational anesthetic agent. Anesth Analg 1975; 54:758-65.
2. Smith I, Nathanson M, White P. Sevoflurane-a long-awaited volatile anaesthetic. Br J Anaesth 1996; 76:435-45.
3. Behne M, Wilke H, Harder S. Clinical pharmacokinetics of sevoflurane [Review]. Clin Pharmacokinet 1999; 36:13-26.
4. Young C, Apfelbaum J. A comparative review of the newer inhalational anaesthetics [Review]. CNS Drugs 1998; 4:287-310.
5. Kharasch E. Biotransformation of sevoflurane. Anesth Analg 1995; 81(Suppl 6):S27-38.
6. Cittanova M, Lelongt B, Verpont M, Geniteau-Legedre M, Wahbe F, Prie D, et al. Fluoride ion toxicity in human kidney collecting duct cells. Anesthesiology 1996;84:428-35.
7. Eger E, Coblin D, Bowland T, Ionescu P, Laster M, Fang Z, et al. Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
8. Strum D, Johnson B, Eger E. Stability of sevoflurane in soda lime. Anesthesiology 1987; 67:779-81.
9. Hanaki C, Fujii K, Morio M, Tashinao T. Decomposition of sevoflurane by soda lime.Hiroshima J Med Sci 1987; 36:61-8.
10. Bito H, Ikeda K. Closed-circuit anesthesia with sevoflurane in humans. Anesthesiology 1994; 80:71-6.
11. Ruzicka J, Hidalgo J, Tinker J, Baker M. Inhibition of volatile sevoflurane degradation product formation in an anesthesia circuit by a reduction in sodalime temperature. Anesthesiology 1994; 81:238-44.
12. Morio M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, et al. Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the by-products. Anesthesiology 1992; 77:1155-64.
13. Gonsowski C, Laster M, Eger E, Ferrel L, Kerschmann R. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
14. Keller K, Callan C, Prokocimer P, Delgedo-Herrera L, Friedman M, Hoffman G, et al. Inhalation toxicity study of a haloalkene degradant of sevoflurane, compound A (PIFE),in Sprague-Dawley rats. Anesthesiology 1995; 83:1220-32.
15. Mazze R, Jamison R. Low-flow (1 L/min) sevoflurane. Is it safe? [Editorial]. Anesthesiology 1997; 86:1225-7.
16. Baum J, Stanke H. Low flow and minimal flow with sevoflurane. Anaesthesist 1998;47(Suppl 1):S70-6.
17. Eger EI II, Koblin DD, Bowland T, et al. Nephrotoxicity of sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
18. Eger EI II, Gong D, Koblin DD, et al. Dose related biochemical markers of renal injury after sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997;85:1154-63.
19.MazzeRI, Friedman M, Delgado-Herrera L, Galvez ST, Mayer DB.Toxicity of compound A plus sevoflurane compared with isoflurane in non-human primates. Anesthesiology 1998; 89:A490
20. C. KEIJZER, R. S. G. M. PEREZ and J. J. DE LANGE. Compound A and carbon monoxide production from sevoflurane and seven different types of carbon dioxide absorbent in a patient model.Acta Anaesthesiol Scand 2007; 51:31-37
21. Versichelen LF et. Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.Anesthesiology. 2001 Sep; 95(3):750-5.
22. Fang ZX, Kandel L, Laster MJ, Ionescu P, Eger El II. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82: 775-81
23.Michael E. Goldberg et al. Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers. Anesth Analg 1999; 88:437-45)
24. Kharasch ED, Thoming DT, Garton K, et al. Role of renal cysteine conjugate S-lyase in the mechanism of compound A nephrotoxicity in rats. Anesthesiology 1997;86:160-71.
25. Bito H, lkeuchi Y, Ikeda K. Effects of low-flow sevoflurane anesthesia on renal function: comparison with high-flow sevoflurane anesthesia and low-flow isoflurane anesthesia. Anesthesiology 1997; 86:1231-7.
26. Kharasch ED, Frink EJ Jr, Zager R, et al. Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
27.Thomas J. Ebert,et al. Absence of Renal and Hepatic Toxicity After Four Hours of 1.25 Minimum Alveolar Anesthetic Concentration Sevoflurane Anesthesia in Volunteers .Anesth Analg 1998; 86:662-7
28. Wallin R, Regan B, Napoli M, Stern I. Sevoflurane: a new inhalational anesthetic agent. Anesth Analg 1975; 54:758-65.
29. Smith I, Nathanson M, White P. Sevoflurane-a long-awaited volatile anaesthetic. Br J Anaesth 1996; 76:435-45.
30. Behne M, Wilke H, Harder S. Clinical pharmacokinetics of sevoflurane [Review]. Clin Pharmacokinet 1999; 36:13-26.
31. Young C, Apfelbaum J. A comparative review of the newer inhalational anaesthetics [Review]. CNS Drugs 1998; 4:287-310.
32. Kharasch E. Biotransformation of sevoflurane. Anesth Analg 1995; 81(Suppl 6):S27-38.
33. Cittanova M, Lelongt B, Verpont M, Geniteau-Legedre M, Wahbe F, Prie D, et al. Fluoride ion toxicity in human kidney collecting duct cells. Anesthesiology 1996;84:428-35.
34. Eger E, Coblin D, Bowland T, Ionescu P, Laster M, Fang Z, et al. Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
35. Strum D, Johnson B, Eger E. Stability of sevoflurane in soda lime. Anesthesiology 1987; 67:779-81.
36. Hanaki C, Fujii K, Morio M, Tashinao T. Decomposition of sevoflurane by soda lime. Hiroshima J Med Sci 1987; 36:61-8.
37. Bito H, Ikeda K. Closed-circuit anesthesia with sevoflurane in humans. Anesthesiology 1994; 80:71-6.
38. Ruzicka J, Hidalgo J, Tinker J, Baker M. Inhibition of volatile sevoflurane degradation product formation in an anesthesia circuit by a reduction in sodalime temperature. Anesthesiology 1994; 81:238-44.
39. Frink E Jr, Malan T, Morgan S, Brown E, Malcomson M, Brown B. Quantification of the degradation products of sevoflurane in two CO2 absorbants during low-flow anesthesia in surgical patients. Anesthesiology 1992; 77:1064-9.
40. Cunningham D, Huang S, Webster J, Mayoral J, Grabenkort R. Sevoflurane degradation to compound A in anaesthesia breathing systems. Br J Anaesth 1996;77:537-43.
41. Bito H, Ikeda K. Long-duration, low-flow sevoflurane anesthesia using two carbon dioxide absorbents. Anesthesiology 1994; 81: 340-5.
42. Wong T, Lerman J. Factors affecting the rate of disappearance of sevoflurane in Baralyme. Can J Anaesth 1992; 39:366-9.
43. Bito H, Ikeuch Y, Ikeda K. Effects of the water content of soda lime on compound A concentration in the anesthesia circuit in sevoflurane anesthesia. Anesthesiology 1998; 88:66-71.
44. Funk W, Grube M, Wild K, Hobbhahn J. Dry soda lime markedly degrades sevoflurane during simulated inhalation induction. Br J Anaesth 1999; 82:193-8.
45. Fang Z, Kandel L, Laster M, Ionescu P, Eger E. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82:775-81.
46. Frink E, Isner R, Malan T, Morgan S, Brown E, Brown B. Sevoflurane degradation product concentrations with soda lime during prolonged anesthesia. J Clin Anesth 1994;6:239-42.
47. Mono M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, et al. Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the by-products. Anesthesiology 1992; 77:1155-64.
48. Gonsowski C, Laster M, Eger E, Ferrel L, Kerschmann R. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
49. Keller K, Callan C, Prokocimer P, Delgedo-Herrera L, Friedman M, Hoffman G, et al. Inhalation toxicity study of a haloalkene degradant of sevoflurane, compound A (PIFE),in Sprague-Dawley rats. Anesthesiology 1995; 83:1220-32.
50. Mazze R, Jamison R. Low-flow (1 L/min) sevoflurane. Is it safe? [Editorial]. Anesthesiology 1997; 86:1225-7.
51. Baum J, Stanke H. Low flow and minimal flow with sevoflurane. Anaesthesist 1998;47(Suppl 1):S70-6.
52. Gonsowski CT, Laster MJ, Eger EI II, et al. Toxicity of compoundA in rats: effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
53. Eger EI II, Koblin DD, Bowland T, et al. Nephrotoxicity of sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
54. Eger EI II, Gong D, Koblin DD, et al. Dose related biochemical markers of renal injury after sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997;85:1154-63.
55.Mazze RI, Friedman M, Delgado-Herrera L, Galvez ST, Mayer DB.Toxicity of compound A plus sevoflurane compared with isoflurane in non-human primates. Anesthesiology 1998; 89:A490
56. C. KEIJZER, R. S. G. M. PEREZ and J. J. DE LANGE. Compound A and carbon monoxide production from sevoflurane and seven different types of carbon dioxide absorbent in a patient model.Acta Anaesthesiol Scand 2007; 51: 31-37
57. Versichelen LF et. Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.Anesthesiology. 2001 Sep; 95(3):750-5.
58.Michael E. Goldberg et al. Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers. Anesth Analg 1999; 88:437-45)
59. Fang ZX, Kandel L, Laster MJ, Ionescu P, Eger El II. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82: 775-81
60. Bito H, lkeuchi Y, Ikeda K. Effects of low-flow sevoflurane anesthesia on renal function: comparison with high-flow sevoflurane anesthesia and low-flow isofiurane anesthesia. Anesthesiology 1997; 86:1231-7.
61 .Kharasch ED, Frink EJ Jr, Zager R, et al. Assessment of low-flow sevoflurane and isofiurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
62.Thomas J. Ebert,et al. Absence of Renal and Hepatic Toxicity After Four Hours of 1.25 Minimum Alveolar Anesthetic Concentration Sevoflurane Anesthesia in Volunteers .Anesth Analg 1998; 86:662-7
63.Mazze RI, et al. The effects of sevoflurane on serum creatinine and blood urea nitrogen concentrations: a retrospective, twenty-two-center, comparative evaluation of renal function in adult surgical patients. Anesth Analg. 2000 Mar; 90(3):505-8.
1. Wallin R, Regan B, Napoli M, Stern I. Sevoflurane: a new inhalational anesthetic agent. Anesth Analg 1975; 54:758-65.
2. Smith I, Nathanson M, White P. Sevoflurane-a long-awaited volatile anaesthetic. Br J Anaesth 1996; 76:435-45.
3. Behne M, Wilke H, Harder S. Clinical pharmacokinetics of sevoflurane [Review]. Clin Pharmacokinet 1999; 36:13-26.
4. Young C, Apfelbaum J. A comparative review of the newer inhalational anaesthetics [Review]. CNS Drugs 1998; 4:287-310.
5 Kharasch E. Biotransformation of sevoflurane. Anesth Analg 1995; 81(Suppl 6):S27-38.
6. Cittanova M, Lelongt B, Verpont M, Geniteau-Legedre M, Wahbe F, Prie D, et al. Fluoride ion toxicity in human kidney collecting duct cells. Anesthesiology 1996;84:428-35.
7. Eger E, Coblin D, Bowland T, Ionescu P, Laster M, Fang Z, et al. Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
8. Strum D, Johnson B, Eger E. Stability of sevoflurane in soda lime. Anesthesiology 1987; 67:779-81.
9. Hanaki C, Fujii K, Morio M, Tashinao T. Decomposition of sevoflurane by soda lime. Hiroshima J Med Sci 1987; 36:61-8.
10. Bito H, Ikeda K. Closed-circuit anesthesia with sevoflurane in humans. Anesthesiology 1994; 80:71-6.
11. Ruzicka J, Hidalgo J, Tinker J, Baker M. Inhibition of volatile sevoflurane degradation product formation in an anesthesia circuit by a reduction in sodalime temperature. Anesthesiology 1994; 81:238-44.
12. Frink E Jr, Malan T, Morgan S, Brown E, Malcomson M, Brown B. Quantification of the degradation products of sevoflurane in two CO2 absorbants during low-flow anesthesia in surgical patients. Anesthesiology 1992; 77:1064-9.
13. Cunningham D, Huang S, Webster J, Mayoral J, Grabenkort R. Sevoflurane degradation to compound A in anaesthesia breathing systems. Br J Anaesth 1996;77:537-43.
14. Bito H, Ikeda K. Long-duration, low-flow sevoflurane anesthesia using two carbon dioxide absorbents. Anesthesiology 1994; 81: 340-5.
15. Wong T, Lerman J. Factors affecting the rate of disappearance of sevoflurane in Baralyme. Can J Anaesth 1992; 39:366-9.
16. Bito H, Ikeuch Y, Ikeda K. Effects of the water content of soda lime on compound A concentration in the anesthesia circuit in sevoflurane anesthesia. Anesthesiology 1998;8:66-71.
17. Funk W, Grube M, Wild K, Hobbhahn J. Dry soda lime markedly degrades sevoflurane during simulated inhalation induction. Br J Anaesth 1999; 82:193-8.
18. Fang Z, Kandel L, Laster M, Ionescu P, Eger E. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82:775-81.
19. Frink E, Isner R, Malan T, Morgan S, Brown E, Brown B. Sevoflurane degradation product concentrations with soda lime during prolonged anesthesia. J Clin Anesth 1994;6:239-42.
20. Morio M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, et al. Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the by-products. Anesthesiology 1992; 77:1155-64.
21. Gonsowski C, Laster M, Eger E, Ferrel L, Kerschmann R. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
22. Keller K, Callan C, Prokocimer P, Delgedo-Herrera L, Friedman M, Hoffman G, et al. Inhalation toxicity study of a haloalkene degradant of sevoflurane, compound A (PIFE),in Sprague-Dawley rats. Anesthesiology 1995; 83:1220-32.
23. Mazze R, Jamison R. Low-flow (1 L/min) sevoflurane. Is it safe? [Editorial]. Anesthesiology 1997; 86:1225-7.
24. Baum J, Stanke H. Low flow and minimal flow with sevoflurane. Anaesthesist 1998;47(Suppl 1):S70-6.
25. Gonsowski CT, Laster MJ, Eger El II, et al. Toxicity of compoundA in rats: effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
26. Eger EI II, Koblin DD, Bowland T, et al. Nephrotoxicity of sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
27. Eger EI II, Gong D, Koblin DD, et al. Dose related biochemical markers of renal injury after sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997;85:1154-63.
28 Mazze RI, Friedman M, Delgado-Herrera L, Galvez ST, Mayer DB.Toxicity of compound A plus sevoflurane compared with isoflurane in non-human primates. Anesthesiology 1998; 89:A490
29. C. KEIJZER, R. S. G. M. PEREZ and J. J. DE LANGE. Compound A and carbon monoxide production from sevoflurane and seven different types of carbon dioxide absorbent in a patient model.Acta Anaesthesiol Scand 2007; 51:31-37
30. Versichelen LF et. Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.Anesthesiology. 2001 Sep; 95(3):750-5.
31.Michael E. Goldberg et al. Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers. Anesth Analg 1999; 88:437-45)
32. Fang ZX, Kandel L, Laster MJ, Ionescu P, Eger EI II. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82: 775-81
33. Bito H, lkeuchi Y, Ikeda K. Effects of low-flow sevoflurane anesthesia on renal function: comparison with high-flow sevoflurane anesthesia and low-flow isoflurane anesthesia. Anesthesiology 1997; 86:1231-7.
34. Kharasch ED, Frink EJ Jr, Zager R, et al. Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
35.Thomas J. Ebert,et al. Absence of Renal and Hepatic Toxicity After Four Hours of 1.25 Minimum Alveolar Anesthetic Concentration Sevoflurane Anesthesia in Volunteers .Anesth Analg 1998; 86:662-7
36.Kharasch ED, Frink EJ Jr, Zagar R, et al. Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
37. Bito H, Ikeuchi Y, Ikeda K. Effects of low-sevoflurane anesthesia on renal function: comparison with high flow sevoflurane anesthesia and low-flow isoflurane anesthesia. Anesthesiology 1997; 86:1231-7.
38.Kharasch ED, Schroeder JL, Sheffels P, Liggitt HD. Influence of sevoflurane on the metabolism and renal effects of compound A in rats. Anesthesiology. 2005 Dec;103(6):1183-8.
2. Smith I, Nathanson M, White P. Sevoflurane-a long-awaited volatile anaesthetic. Br J Anaesth 1996; 76:435-45.
3. Behne M, Wilke H, Harder S. Clinical pharmacokinetics of sevoflurane [Review]. Clin Pharmacokinet 1999; 36:13-26.
4. Young C, Apfelbaum J. A comparative review of the newer inhalational anaesthetics [Review]. CNS Drugs 1998; 4:287-310.
5. Kharasch E. Biotransformation of sevoflurane. Anesth Analg 1995; 81(Suppl 6):S27-38.
6. Cittanova M, Lelongt B, Verpont M, Geniteau-Legedre M, Wahbe F, Prie D, et al. Fluoride ion toxicity in human kidney collecting duct cells. Anesthesiology 1996;84:428-35.
7. Eger E, Coblin D, Bowland T, Ionescu P, Laster M, Fang Z, et al. Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
8. Strum D, Johnson B, Eger E. Stability of sevoflurane in soda lime. Anesthesiology 1987; 67:779-81.
9. Hanaki C, Fujii K, Morio M, Tashinao T. Decomposition of sevoflurane by soda lime.Hiroshima J Med Sci 1987; 36:61-8.
10. Bito H, Ikeda K. Closed-circuit anesthesia with sevoflurane in humans. Anesthesiology 1994; 80:71-6.
11. Ruzicka J, Hidalgo J, Tinker J, Baker M. Inhibition of volatile sevoflurane degradation product formation in an anesthesia circuit by a reduction in sodalime temperature. Anesthesiology 1994; 81:238-44.
12. Morio M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, et al. Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the by-products. Anesthesiology 1992; 77:1155-64.
13. Gonsowski C, Laster M, Eger E, Ferrel L, Kerschmann R. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
14. Keller K, Callan C, Prokocimer P, Delgedo-Herrera L, Friedman M, Hoffman G, et al. Inhalation toxicity study of a haloalkene degradant of sevoflurane, compound A (PIFE),in Sprague-Dawley rats. Anesthesiology 1995; 83:1220-32.
15. Mazze R, Jamison R. Low-flow (1 L/min) sevoflurane. Is it safe? [Editorial]. Anesthesiology 1997; 86:1225-7.
16. Baum J, Stanke H. Low flow and minimal flow with sevoflurane. Anaesthesist 1998;47(Suppl 1):S70-6.
17. Eger EI II, Koblin DD, Bowland T, et al. Nephrotoxicity of sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
18. Eger EI II, Gong D, Koblin DD, et al. Dose related biochemical markers of renal injury after sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997;85:1154-63.
19.MazzeRI, Friedman M, Delgado-Herrera L, Galvez ST, Mayer DB.Toxicity of compound A plus sevoflurane compared with isoflurane in non-human primates. Anesthesiology 1998; 89:A490
20. C. KEIJZER, R. S. G. M. PEREZ and J. J. DE LANGE. Compound A and carbon monoxide production from sevoflurane and seven different types of carbon dioxide absorbent in a patient model.Acta Anaesthesiol Scand 2007; 51:31-37
21. Versichelen LF et. Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.Anesthesiology. 2001 Sep; 95(3):750-5.
22. Fang ZX, Kandel L, Laster MJ, Ionescu P, Eger El II. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82: 775-81
23.Michael E. Goldberg et al. Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers. Anesth Analg 1999; 88:437-45)
24. Kharasch ED, Thoming DT, Garton K, et al. Role of renal cysteine conjugate S-lyase in the mechanism of compound A nephrotoxicity in rats. Anesthesiology 1997;86:160-71.
25. Bito H, lkeuchi Y, Ikeda K. Effects of low-flow sevoflurane anesthesia on renal function: comparison with high-flow sevoflurane anesthesia and low-flow isoflurane anesthesia. Anesthesiology 1997; 86:1231-7.
26. Kharasch ED, Frink EJ Jr, Zager R, et al. Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
27.Thomas J. Ebert,et al. Absence of Renal and Hepatic Toxicity After Four Hours of 1.25 Minimum Alveolar Anesthetic Concentration Sevoflurane Anesthesia in Volunteers .Anesth Analg 1998; 86:662-7
28. Wallin R, Regan B, Napoli M, Stern I. Sevoflurane: a new inhalational anesthetic agent. Anesth Analg 1975; 54:758-65.
29. Smith I, Nathanson M, White P. Sevoflurane-a long-awaited volatile anaesthetic. Br J Anaesth 1996; 76:435-45.
30. Behne M, Wilke H, Harder S. Clinical pharmacokinetics of sevoflurane [Review]. Clin Pharmacokinet 1999; 36:13-26.
31. Young C, Apfelbaum J. A comparative review of the newer inhalational anaesthetics [Review]. CNS Drugs 1998; 4:287-310.
32. Kharasch E. Biotransformation of sevoflurane. Anesth Analg 1995; 81(Suppl 6):S27-38.
33. Cittanova M, Lelongt B, Verpont M, Geniteau-Legedre M, Wahbe F, Prie D, et al. Fluoride ion toxicity in human kidney collecting duct cells. Anesthesiology 1996;84:428-35.
34. Eger E, Coblin D, Bowland T, Ionescu P, Laster M, Fang Z, et al. Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
35. Strum D, Johnson B, Eger E. Stability of sevoflurane in soda lime. Anesthesiology 1987; 67:779-81.
36. Hanaki C, Fujii K, Morio M, Tashinao T. Decomposition of sevoflurane by soda lime. Hiroshima J Med Sci 1987; 36:61-8.
37. Bito H, Ikeda K. Closed-circuit anesthesia with sevoflurane in humans. Anesthesiology 1994; 80:71-6.
38. Ruzicka J, Hidalgo J, Tinker J, Baker M. Inhibition of volatile sevoflurane degradation product formation in an anesthesia circuit by a reduction in sodalime temperature. Anesthesiology 1994; 81:238-44.
39. Frink E Jr, Malan T, Morgan S, Brown E, Malcomson M, Brown B. Quantification of the degradation products of sevoflurane in two CO2 absorbants during low-flow anesthesia in surgical patients. Anesthesiology 1992; 77:1064-9.
40. Cunningham D, Huang S, Webster J, Mayoral J, Grabenkort R. Sevoflurane degradation to compound A in anaesthesia breathing systems. Br J Anaesth 1996;77:537-43.
41. Bito H, Ikeda K. Long-duration, low-flow sevoflurane anesthesia using two carbon dioxide absorbents. Anesthesiology 1994; 81: 340-5.
42. Wong T, Lerman J. Factors affecting the rate of disappearance of sevoflurane in Baralyme. Can J Anaesth 1992; 39:366-9.
43. Bito H, Ikeuch Y, Ikeda K. Effects of the water content of soda lime on compound A concentration in the anesthesia circuit in sevoflurane anesthesia. Anesthesiology 1998; 88:66-71.
44. Funk W, Grube M, Wild K, Hobbhahn J. Dry soda lime markedly degrades sevoflurane during simulated inhalation induction. Br J Anaesth 1999; 82:193-8.
45. Fang Z, Kandel L, Laster M, Ionescu P, Eger E. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82:775-81.
46. Frink E, Isner R, Malan T, Morgan S, Brown E, Brown B. Sevoflurane degradation product concentrations with soda lime during prolonged anesthesia. J Clin Anesth 1994;6:239-42.
47. Mono M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, et al. Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the by-products. Anesthesiology 1992; 77:1155-64.
48. Gonsowski C, Laster M, Eger E, Ferrel L, Kerschmann R. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
49. Keller K, Callan C, Prokocimer P, Delgedo-Herrera L, Friedman M, Hoffman G, et al. Inhalation toxicity study of a haloalkene degradant of sevoflurane, compound A (PIFE),in Sprague-Dawley rats. Anesthesiology 1995; 83:1220-32.
50. Mazze R, Jamison R. Low-flow (1 L/min) sevoflurane. Is it safe? [Editorial]. Anesthesiology 1997; 86:1225-7.
51. Baum J, Stanke H. Low flow and minimal flow with sevoflurane. Anaesthesist 1998;47(Suppl 1):S70-6.
52. Gonsowski CT, Laster MJ, Eger EI II, et al. Toxicity of compoundA in rats: effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
53. Eger EI II, Koblin DD, Bowland T, et al. Nephrotoxicity of sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
54. Eger EI II, Gong D, Koblin DD, et al. Dose related biochemical markers of renal injury after sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997;85:1154-63.
55.Mazze RI, Friedman M, Delgado-Herrera L, Galvez ST, Mayer DB.Toxicity of compound A plus sevoflurane compared with isoflurane in non-human primates. Anesthesiology 1998; 89:A490
56. C. KEIJZER, R. S. G. M. PEREZ and J. J. DE LANGE. Compound A and carbon monoxide production from sevoflurane and seven different types of carbon dioxide absorbent in a patient model.Acta Anaesthesiol Scand 2007; 51: 31-37
57. Versichelen LF et. Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.Anesthesiology. 2001 Sep; 95(3):750-5.
58.Michael E. Goldberg et al. Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers. Anesth Analg 1999; 88:437-45)
59. Fang ZX, Kandel L, Laster MJ, Ionescu P, Eger El II. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82: 775-81
60. Bito H, lkeuchi Y, Ikeda K. Effects of low-flow sevoflurane anesthesia on renal function: comparison with high-flow sevoflurane anesthesia and low-flow isofiurane anesthesia. Anesthesiology 1997; 86:1231-7.
61 .Kharasch ED, Frink EJ Jr, Zager R, et al. Assessment of low-flow sevoflurane and isofiurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
62.Thomas J. Ebert,et al. Absence of Renal and Hepatic Toxicity After Four Hours of 1.25 Minimum Alveolar Anesthetic Concentration Sevoflurane Anesthesia in Volunteers .Anesth Analg 1998; 86:662-7
63.Mazze RI, et al. The effects of sevoflurane on serum creatinine and blood urea nitrogen concentrations: a retrospective, twenty-two-center, comparative evaluation of renal function in adult surgical patients. Anesth Analg. 2000 Mar; 90(3):505-8.
1. Wallin R, Regan B, Napoli M, Stern I. Sevoflurane: a new inhalational anesthetic agent. Anesth Analg 1975; 54:758-65.
2. Smith I, Nathanson M, White P. Sevoflurane-a long-awaited volatile anaesthetic. Br J Anaesth 1996; 76:435-45.
3. Behne M, Wilke H, Harder S. Clinical pharmacokinetics of sevoflurane [Review]. Clin Pharmacokinet 1999; 36:13-26.
4. Young C, Apfelbaum J. A comparative review of the newer inhalational anaesthetics [Review]. CNS Drugs 1998; 4:287-310.
5 Kharasch E. Biotransformation of sevoflurane. Anesth Analg 1995; 81(Suppl 6):S27-38.
6. Cittanova M, Lelongt B, Verpont M, Geniteau-Legedre M, Wahbe F, Prie D, et al. Fluoride ion toxicity in human kidney collecting duct cells. Anesthesiology 1996;84:428-35.
7. Eger E, Coblin D, Bowland T, Ionescu P, Laster M, Fang Z, et al. Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
8. Strum D, Johnson B, Eger E. Stability of sevoflurane in soda lime. Anesthesiology 1987; 67:779-81.
9. Hanaki C, Fujii K, Morio M, Tashinao T. Decomposition of sevoflurane by soda lime. Hiroshima J Med Sci 1987; 36:61-8.
10. Bito H, Ikeda K. Closed-circuit anesthesia with sevoflurane in humans. Anesthesiology 1994; 80:71-6.
11. Ruzicka J, Hidalgo J, Tinker J, Baker M. Inhibition of volatile sevoflurane degradation product formation in an anesthesia circuit by a reduction in sodalime temperature. Anesthesiology 1994; 81:238-44.
12. Frink E Jr, Malan T, Morgan S, Brown E, Malcomson M, Brown B. Quantification of the degradation products of sevoflurane in two CO2 absorbants during low-flow anesthesia in surgical patients. Anesthesiology 1992; 77:1064-9.
13. Cunningham D, Huang S, Webster J, Mayoral J, Grabenkort R. Sevoflurane degradation to compound A in anaesthesia breathing systems. Br J Anaesth 1996;77:537-43.
14. Bito H, Ikeda K. Long-duration, low-flow sevoflurane anesthesia using two carbon dioxide absorbents. Anesthesiology 1994; 81: 340-5.
15. Wong T, Lerman J. Factors affecting the rate of disappearance of sevoflurane in Baralyme. Can J Anaesth 1992; 39:366-9.
16. Bito H, Ikeuch Y, Ikeda K. Effects of the water content of soda lime on compound A concentration in the anesthesia circuit in sevoflurane anesthesia. Anesthesiology 1998;8:66-71.
17. Funk W, Grube M, Wild K, Hobbhahn J. Dry soda lime markedly degrades sevoflurane during simulated inhalation induction. Br J Anaesth 1999; 82:193-8.
18. Fang Z, Kandel L, Laster M, Ionescu P, Eger E. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82:775-81.
19. Frink E, Isner R, Malan T, Morgan S, Brown E, Brown B. Sevoflurane degradation product concentrations with soda lime during prolonged anesthesia. J Clin Anesth 1994;6:239-42.
20. Morio M, Fujii K, Satoh N, Imai M, Kawakami U, Mizuno T, et al. Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the by-products. Anesthesiology 1992; 77:1155-64.
21. Gonsowski C, Laster M, Eger E, Ferrel L, Kerschmann R. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
22. Keller K, Callan C, Prokocimer P, Delgedo-Herrera L, Friedman M, Hoffman G, et al. Inhalation toxicity study of a haloalkene degradant of sevoflurane, compound A (PIFE),in Sprague-Dawley rats. Anesthesiology 1995; 83:1220-32.
23. Mazze R, Jamison R. Low-flow (1 L/min) sevoflurane. Is it safe? [Editorial]. Anesthesiology 1997; 86:1225-7.
24. Baum J, Stanke H. Low flow and minimal flow with sevoflurane. Anaesthesist 1998;47(Suppl 1):S70-6.
25. Gonsowski CT, Laster MJ, Eger El II, et al. Toxicity of compoundA in rats: effect of a 3-hour administration. Anesthesiology 1994; 80:556-65.
26. Eger EI II, Koblin DD, Bowland T, et al. Nephrotoxicity of sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997; 84:160-8.
27. Eger EI II, Gong D, Koblin DD, et al. Dose related biochemical markers of renal injury after sevoflurane vs. desflurane anesthesia in volunteers. Anesth Analg 1997;85:1154-63.
28 Mazze RI, Friedman M, Delgado-Herrera L, Galvez ST, Mayer DB.Toxicity of compound A plus sevoflurane compared with isoflurane in non-human primates. Anesthesiology 1998; 89:A490
29. C. KEIJZER, R. S. G. M. PEREZ and J. J. DE LANGE. Compound A and carbon monoxide production from sevoflurane and seven different types of carbon dioxide absorbent in a patient model.Acta Anaesthesiol Scand 2007; 51:31-37
30. Versichelen LF et. Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.Anesthesiology. 2001 Sep; 95(3):750-5.
31.Michael E. Goldberg et al. Dose of Compound A, Not Sevoflurane, Determines Changes in the Biochemical Markers of Renal Injury in Healthy Volunteers. Anesth Analg 1999; 88:437-45)
32. Fang ZX, Kandel L, Laster MJ, Ionescu P, Eger EI II. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme? and soda lime. Anesth Analg 1996; 82: 775-81
33. Bito H, lkeuchi Y, Ikeda K. Effects of low-flow sevoflurane anesthesia on renal function: comparison with high-flow sevoflurane anesthesia and low-flow isoflurane anesthesia. Anesthesiology 1997; 86:1231-7.
34. Kharasch ED, Frink EJ Jr, Zager R, et al. Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
35.Thomas J. Ebert,et al. Absence of Renal and Hepatic Toxicity After Four Hours of 1.25 Minimum Alveolar Anesthetic Concentration Sevoflurane Anesthesia in Volunteers .Anesth Analg 1998; 86:662-7
36.Kharasch ED, Frink EJ Jr, Zagar R, et al. Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity. Anesthesiology 1997; 86: 1238-53.
37. Bito H, Ikeuchi Y, Ikeda K. Effects of low-sevoflurane anesthesia on renal function: comparison with high flow sevoflurane anesthesia and low-flow isoflurane anesthesia. Anesthesiology 1997; 86:1231-7.
38.Kharasch ED, Schroeder JL, Sheffels P, Liggitt HD. Influence of sevoflurane on the metabolism and renal effects of compound A in rats. Anesthesiology. 2005 Dec;103(6):1183-8.