血容量变化对血浆异丙酚浓度影响的试验研究
摘要
[目的]自异丙酚应用于临床以来,已有大量的与之相关的临床药动学和药效学的文献报道。但到目前为止,涉及到低血容量性休克和超容量血液稀释对异丙酚药动学和药效学影响的报道较为少见,而这些又是临床麻醉中所经常面临的实际问题。因此,对这些课题深入的了解有助于指导临床麻醉的合理用药和减少麻醉药的副反应。本试验以猪为受试对象旨在观察和探讨:1)低血容量性休克的发展历程对血浆异丙酚浓度的影响;2)低血容量性休克的不同阶段对血浆异丙酚浓度的影响;3)失血量与血浆异丙酚浓度的相关性:4)低血容量性休克对肝脏异丙酚摄取和代谢的影响;5)大容量超容量血液稀释对心脏功能的影响;6)大容量超容量血液稀释对血浆异丙酚浓度的影响;7)大容量超容量血液稀释后的血浆增量效应的变化;8)大容量超容量血液稀释对机体氧供耗平衡的影响。
尽管在我国高效液相检测人血浆异丙酚的技术已经成熟,但前期的预试验发现将其应用于检测大动物血浆异丙酚时有明显的局限性。为能顺利的完成本试验的研究,建立起检测猪血浆异丙酚浓度的方法是本课题的关键,因此,需要在借鉴常用的高效液相检测方法的基础上,通过对实验条件的调整使之更适合于检测猪血浆中的异丙酚。另外,创立一种新的异丙酚检测技术—高效毛细管电泳法检测异丙酚的方法,并对该方法进行客观评价。
本研究包括三个部分。第一部分:异丙酚药物浓度检测方法的建立:第二部分:低血容量性休克对血浆异丙酚浓度的影响;第三部分:超容量血液稀释对血浆容量及异丙酚浓度的影响。
新扮医科大学临床医学博d匕学位论文
【方法】第一部分:对常用的高效液相检测血浆异丙酚方法的实
验条件进行测试和调整,目的在于避免预试验中出现的乳化现象、提
取时间过长、绝对提取率低和不稳定以及改变流动相以获得较好的峰
形。试验中考察和比较了用乙醚替代其他萃取有机溶剂、三乙胺乙醇
替代其他碱性有机溶液和在甲醇一水组成的流动相中加入p一环糊精
的结果。另外,还建立了异丙酚毛细管电泳的分离方法及条件,包括
运行缓冲液的pH值、运行缓冲液的组分和运行电压等。
第二部分:连续输注异丙酚达到稳定的血药浓度后,每隔30min
间断放出10%的预计血容量直至循环衰竭。分别以外周血管阻力和心
率表示休克代偿期的指标;平均动脉压低于50mmHg并且不能维持判
断为循环衰竭;动脉与肝静脉异丙酚浓度的差值间接反应肝脏对异丙
酚的代谢清除能力,同时对低血容量性休克中的动脉异丙酚浓度进行
观察。
第三部分:由于新型胶体溶液对凝血机制的干扰越来越轻,这就
为临床实施超容量血液稀释中进一步增加胶体液的容量留下了空间。
因此在第三部分的研究中应用6%轻乙基淀粉30ml·kg一,(临床常
用巧一20 ml·kg一l)输注30min,模拟临床中超容量血液稀释的方法。
利用肺动脉导管技术评价心血管功能;观察被稀释后红细胞压积的动
态变化,评价超容后的血浆容量变化;以及观察超容后的氧供耗平衡
和动脉血浆异丙酚浓度的变化。
【结果】第一部分:确立了以磨香草酚为内标物;乙醚为萃取有
机溶剂和在甲醇一水的流动相中加入p一环糊精:选用Agilent
ZORBAX Extend一C 18色谱柱进行分离;检测波长为273nm,作为高效
液相分离异丙酚的基本检测条件。结果血浆异丙酚的最低检测线为
0.10 09·ml一‘;绝对提取率超过85%;血浆异丙酚在0.1一4.0 09·ml一’
浓度范围内线性关系良好(:=0.9998),回归方程Y二2.68 x 10一3x+5.58
xlo一。该方法避免了萃取过程中的乳化现象,大大减少了对异丙酚
的提取时间。
通过对异丙酚毛细管电泳分离方法及条件的考察,最终确立了以
赓香草酚为内标;检测波长27Onm;电泳条件:石英毛细管柱(75协
一2一
中文摘要
mx37em);运行缓冲液为:300pl乙睛+200协lp一环糊精+500,
ISDS+500“l磷酸缓冲液;分离电压为10KV;毛细管柱温为25℃等,
作为毛细管电泳的分离方法和条件。结果异丙酚在1一16 09·ml一,浓
度范围内线性关系良好(r=0.9991),回归方程Y=5.574X一0.3933;平
均加样回收率为101.1%;药物检测限为0.spg·ml一‘:血浆异丙酚检
测限为25 09·ml一,。
第二部分:结果表明,放血量小于30%的预计血容量,动脉异丙
酚浓度与基础值(l .18士0.2409·ml一,)比较无显著改变。当放血量
超过30%的预计血容量和循环衰竭时动脉异丙酚浓度迅速增高;外周
血管阻力达到最大值,动脉异丙酚浓度(1,37士0.38 09·ml一‘)比基
础值增加117%,心率达到最大值,动脉异丙酚浓度(2.01士o.58p
g·ml一l)比基础值增加171%,循环衰竭时动脉异丙酚浓度(2.91士
0.46 09·ml一,)是放血前的2.47倍;放血量超过40%的预计血容量
以后,动脉异丙酚浓度与放血量呈直线相关(r=0.75),动脉一肝静脉
异丙酚浓度差值明显减小,提示肝脏对异丙酚的代谢清除能力开始降
低。
第三部分:结果表明,大容量超容量血液稀释后所有受试动物均
可耐受,无并发症出现。超容后红细胞压积由基础值28士4%降至16
土3%,血浆容量比基础容量增加43%,30min后血浆容量的扩增效
应明显减弱降至25%,以后降幅减小;超容后各时点的平均动脉压和
心率与基础值比较,无显著变化,超容结束后中心静脉压和肺毛细血
管嵌压?
[Objectives] Since propofol has been used in clinical anesthesia, many scientists investigated its pharmacodynamic and pharmacokinetic aspects. However, influence of hypovolemia and hypervolemic hemodilu-tion on the amplitude of plasma propofol concentration has not yet been fully investigated during continuous propofol infusion, and they were a practical problem that an anesthesiologist often faced to. Therefore, an experimental research on pigs were taken place to discuss following fields: 1) Efficacy of the development of hypovolemic shock on the plasma propofol concentration; 2 ) Efficacy of different stages of hypovolemic shock on plasma propofol concentration; 3) Correlation between blood volume lost and plasma propofol concentration; 4) Efficacy of hypovole- mic shock on the clearance and metabolism of propofol by liver; 5)Efficacy of hypervolemic hemodilution on myocar-dial function and analysis of feasibility; 6)Efficacy of hypervolemic hemodilution on plasma propofol concentration; 7)Efficacy of hypervolemic hemodilution on plasma incremental effect; 8)Efficacy of hypervolemic hemodilution on the balance of supply and consumption of oxygen.Even the high performance liquid chromatography (HPLC) was one of the sophisticated method for measurement of propofol in human plasma concentration, it showed an obvious limitation for measurement of propofol plasma concentration in large animals during the pre-experiment.
HPLC measuring conditions should be adjusted and evaluated for the proper measurment of propofol plasma concentration in pigs.This experimental study can be summarized in three parts. Part 1: Establishment of measuring.method for propofol concentration. Part 2: Efficacy of hypovolemic shock against plasma propofol concentration. Part 3: Efficacy of hypervolemic hemodilution on plasma volume and plasma propofol concentration.[ Methods ] In part 1 ,in order to avoid the malpractice which occurred in pre-experimental study, such as emulsifying affection, prolonged extracting time, low absolute extracting rate and instability, adjustment of detecting conditions were taken place and mobile phase changed for a better formation of peaks. Observation of aether and ethanol triethylamine as substitutes for other extract organic and alky organic solutions, and addtion of β -cyclodextrin in mobile phase consisted of methyl hydrate and water. Electrophoretic separation for propofol was also been established, including pH value of buffering solution and its subdivision and working voltage.In Part 2, after a stable propofol plasma concentration was achieved by continuous propofol infusion, and stepwise bleeding of each ten percentage blood volume was taken every 30 min, thereafter, to the point of circulatory collapse. Systemic vascular resistance(SVR) and heart rate(HR) were counted for shock compensatory indicators; mean arterial pressure lower 50mmHg and could not insist on consideration as circulatory collapse; difference between arterial and hepatic vein concentrations of propofol reflects the clearance ability of propofol in liver indirectly and the arterial propofol concentration was detected during all the procedure against hypovolemic shock.In Part 3,The less interruption of new colloid solutions against the coagulating system may gives further space to increase the colloid solution volume during hypervolemic hemodilution. 6% hetastarch was
infused in 30 minutes with 30ml/kg dosage (common clinical was between 15~20 ml/kg dosage), for stimulation of the hypervolemic hemodilution in clinical practice. Cardiovascular function was evaluated by pulmonary artery catheter; posthypervolemic plasma volume changes was estimated by hematocrit dynamic changes; the posthypervolemic supply and consumption balance of oxygen and arterial propofol concentration were also observed.[Results] In Part 1, Propofol in pigs plasma was extracted with Aether and thymol was used as the internal standard, ethanol triethylamine was employed as substitute for the extraction in organic solutions, β -cyclodextrin in mobile phase consi
尽管在我国高效液相检测人血浆异丙酚的技术已经成熟,但前期的预试验发现将其应用于检测大动物血浆异丙酚时有明显的局限性。为能顺利的完成本试验的研究,建立起检测猪血浆异丙酚浓度的方法是本课题的关键,因此,需要在借鉴常用的高效液相检测方法的基础上,通过对实验条件的调整使之更适合于检测猪血浆中的异丙酚。另外,创立一种新的异丙酚检测技术—高效毛细管电泳法检测异丙酚的方法,并对该方法进行客观评价。
本研究包括三个部分。第一部分:异丙酚药物浓度检测方法的建立:第二部分:低血容量性休克对血浆异丙酚浓度的影响;第三部分:超容量血液稀释对血浆容量及异丙酚浓度的影响。
新扮医科大学临床医学博d匕学位论文
【方法】第一部分:对常用的高效液相检测血浆异丙酚方法的实
验条件进行测试和调整,目的在于避免预试验中出现的乳化现象、提
取时间过长、绝对提取率低和不稳定以及改变流动相以获得较好的峰
形。试验中考察和比较了用乙醚替代其他萃取有机溶剂、三乙胺乙醇
替代其他碱性有机溶液和在甲醇一水组成的流动相中加入p一环糊精
的结果。另外,还建立了异丙酚毛细管电泳的分离方法及条件,包括
运行缓冲液的pH值、运行缓冲液的组分和运行电压等。
第二部分:连续输注异丙酚达到稳定的血药浓度后,每隔30min
间断放出10%的预计血容量直至循环衰竭。分别以外周血管阻力和心
率表示休克代偿期的指标;平均动脉压低于50mmHg并且不能维持判
断为循环衰竭;动脉与肝静脉异丙酚浓度的差值间接反应肝脏对异丙
酚的代谢清除能力,同时对低血容量性休克中的动脉异丙酚浓度进行
观察。
第三部分:由于新型胶体溶液对凝血机制的干扰越来越轻,这就
为临床实施超容量血液稀释中进一步增加胶体液的容量留下了空间。
因此在第三部分的研究中应用6%轻乙基淀粉30ml·kg一,(临床常
用巧一20 ml·kg一l)输注30min,模拟临床中超容量血液稀释的方法。
利用肺动脉导管技术评价心血管功能;观察被稀释后红细胞压积的动
态变化,评价超容后的血浆容量变化;以及观察超容后的氧供耗平衡
和动脉血浆异丙酚浓度的变化。
【结果】第一部分:确立了以磨香草酚为内标物;乙醚为萃取有
机溶剂和在甲醇一水的流动相中加入p一环糊精:选用Agilent
ZORBAX Extend一C 18色谱柱进行分离;检测波长为273nm,作为高效
液相分离异丙酚的基本检测条件。结果血浆异丙酚的最低检测线为
0.10 09·ml一‘;绝对提取率超过85%;血浆异丙酚在0.1一4.0 09·ml一’
浓度范围内线性关系良好(:=0.9998),回归方程Y二2.68 x 10一3x+5.58
xlo一。该方法避免了萃取过程中的乳化现象,大大减少了对异丙酚
的提取时间。
通过对异丙酚毛细管电泳分离方法及条件的考察,最终确立了以
赓香草酚为内标;检测波长27Onm;电泳条件:石英毛细管柱(75协
一2一
中文摘要
mx37em);运行缓冲液为:300pl乙睛+200协lp一环糊精+500,
ISDS+500“l磷酸缓冲液;分离电压为10KV;毛细管柱温为25℃等,
作为毛细管电泳的分离方法和条件。结果异丙酚在1一16 09·ml一,浓
度范围内线性关系良好(r=0.9991),回归方程Y=5.574X一0.3933;平
均加样回收率为101.1%;药物检测限为0.spg·ml一‘:血浆异丙酚检
测限为25 09·ml一,。
第二部分:结果表明,放血量小于30%的预计血容量,动脉异丙
酚浓度与基础值(l .18士0.2409·ml一,)比较无显著改变。当放血量
超过30%的预计血容量和循环衰竭时动脉异丙酚浓度迅速增高;外周
血管阻力达到最大值,动脉异丙酚浓度(1,37士0.38 09·ml一‘)比基
础值增加117%,心率达到最大值,动脉异丙酚浓度(2.01士o.58p
g·ml一l)比基础值增加171%,循环衰竭时动脉异丙酚浓度(2.91士
0.46 09·ml一,)是放血前的2.47倍;放血量超过40%的预计血容量
以后,动脉异丙酚浓度与放血量呈直线相关(r=0.75),动脉一肝静脉
异丙酚浓度差值明显减小,提示肝脏对异丙酚的代谢清除能力开始降
低。
第三部分:结果表明,大容量超容量血液稀释后所有受试动物均
可耐受,无并发症出现。超容后红细胞压积由基础值28士4%降至16
土3%,血浆容量比基础容量增加43%,30min后血浆容量的扩增效
应明显减弱降至25%,以后降幅减小;超容后各时点的平均动脉压和
心率与基础值比较,无显著变化,超容结束后中心静脉压和肺毛细血
管嵌压?
[Objectives] Since propofol has been used in clinical anesthesia, many scientists investigated its pharmacodynamic and pharmacokinetic aspects. However, influence of hypovolemia and hypervolemic hemodilu-tion on the amplitude of plasma propofol concentration has not yet been fully investigated during continuous propofol infusion, and they were a practical problem that an anesthesiologist often faced to. Therefore, an experimental research on pigs were taken place to discuss following fields: 1) Efficacy of the development of hypovolemic shock on the plasma propofol concentration; 2 ) Efficacy of different stages of hypovolemic shock on plasma propofol concentration; 3) Correlation between blood volume lost and plasma propofol concentration; 4) Efficacy of hypovole- mic shock on the clearance and metabolism of propofol by liver; 5)Efficacy of hypervolemic hemodilution on myocar-dial function and analysis of feasibility; 6)Efficacy of hypervolemic hemodilution on plasma propofol concentration; 7)Efficacy of hypervolemic hemodilution on plasma incremental effect; 8)Efficacy of hypervolemic hemodilution on the balance of supply and consumption of oxygen.Even the high performance liquid chromatography (HPLC) was one of the sophisticated method for measurement of propofol in human plasma concentration, it showed an obvious limitation for measurement of propofol plasma concentration in large animals during the pre-experiment.
HPLC measuring conditions should be adjusted and evaluated for the proper measurment of propofol plasma concentration in pigs.This experimental study can be summarized in three parts. Part 1: Establishment of measuring.method for propofol concentration. Part 2: Efficacy of hypovolemic shock against plasma propofol concentration. Part 3: Efficacy of hypervolemic hemodilution on plasma volume and plasma propofol concentration.[ Methods ] In part 1 ,in order to avoid the malpractice which occurred in pre-experimental study, such as emulsifying affection, prolonged extracting time, low absolute extracting rate and instability, adjustment of detecting conditions were taken place and mobile phase changed for a better formation of peaks. Observation of aether and ethanol triethylamine as substitutes for other extract organic and alky organic solutions, and addtion of β -cyclodextrin in mobile phase consisted of methyl hydrate and water. Electrophoretic separation for propofol was also been established, including pH value of buffering solution and its subdivision and working voltage.In Part 2, after a stable propofol plasma concentration was achieved by continuous propofol infusion, and stepwise bleeding of each ten percentage blood volume was taken every 30 min, thereafter, to the point of circulatory collapse. Systemic vascular resistance(SVR) and heart rate(HR) were counted for shock compensatory indicators; mean arterial pressure lower 50mmHg and could not insist on consideration as circulatory collapse; difference between arterial and hepatic vein concentrations of propofol reflects the clearance ability of propofol in liver indirectly and the arterial propofol concentration was detected during all the procedure against hypovolemic shock.In Part 3,The less interruption of new colloid solutions against the coagulating system may gives further space to increase the colloid solution volume during hypervolemic hemodilution. 6% hetastarch was
infused in 30 minutes with 30ml/kg dosage (common clinical was between 15~20 ml/kg dosage), for stimulation of the hypervolemic hemodilution in clinical practice. Cardiovascular function was evaluated by pulmonary artery catheter; posthypervolemic plasma volume changes was estimated by hematocrit dynamic changes; the posthypervolemic supply and consumption balance of oxygen and arterial propofol concentration were also observed.[Results] In Part 1, Propofol in pigs plasma was extracted with Aether and thymol was used as the internal standard, ethanol triethylamine was employed as substitute for the extraction in organic solutions, β -cyclodextrin in mobile phase consi
引文
[1] 李正翔,王舒,张素品,等.高效液相色谱法测定人血清中的异丙酚浓度.中国医院药学杂志1997,17(7);293-95.
[2] 张燕婉,刘进,赵延.高效液相色谱法测定人血浆中丙泊酚浓度.中国药学杂志1999;34(12):831-833.
[3] 蒋硕民,王增寿,金盛威,等.反相高效液相色谱法测定异丙酚血清浓度.中国药房2001;12(3);161-62.
[4] 屠建中,吴丽花,章霞等.高效液相色谱-荧光检测法测定异丙酚的血药浓度.药物分析杂志2002;22(1):65-67.
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[6] Cockshott ID, Douglas EJ, Plummer GF, Simons PJ: The pharmacokinetics of propofol in laboratory animals. Xenobiotica 1992; 22: 369-75
[7] 陈介克,主编.毛细管电泳色谱及其应用.北京:科学出版社,2001.3-4.
[8] Johnson KB, Egan TD, Kem SE, et al: The influence of hemorrhagic shock on propofol: A pharmacokinetic and pharmacodynamic analysisi. Anesthesiology 2003; 99: 409-20.
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[11] Weiskopf RB, Bogetz MS. Haemorrhage decreases the anaesthetic requirement for ketamine and thiopentone in the pig. Br J Anaesth 1985; 57: 1022-5.
[12] Adams P, Gelman S, Reves JG, Greenblatt DJ, Alvis JM, Bradley E: Midazolam pharmacodynamics and pharmacokinetics during acute hypovolemia. Anesthesiology 1985; 63: 140-6.
[13]Klockowski PM, Levy G: Kinetics of drug action in disease states. XXV. Effect of experimental hypovolemia on the pharmacodynamics and pharmacokinetics of desmethyldiazepam. J Pharmacol Exp Ther 1988; 245:508-12.
[14]Egan TD, Kuramkote S, Gong G, Zhang J, McJames SW, Bailey PL: Fentanyl pharmacokinetics in hemorrhagic shock: a porcine model. Anesthesiology 1999; 91:156-66.
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[17]Ludbrook J: Hemorrhage and shock, Cardiovascular Reflex Control in Health and Disease. Edited by Hainsworth R, Mark AL. London, WB Saunders, 1993, pp 463-90.
[18]Bellamy RF, Maningas PA, Wenger BA: Current shock models and clinical correlations. Ann Emerg Med 1986; 15:1392-5.
[19]McDaniel LB,ZwischenbergerJB,Vertrees RA,et al. Mixed Venous Oxygen Saturation During Cardiopulmonary Bypass Poorly Predicts Regional Venous Saturation. Anesth Analg 1995; 80:466-472.
[20]Lundeen G, Manohar M, Parks C: Systemic distribution of blood flow in swine while awake and during 1.0 and 1.5 MAC isoflurane anesthesia with or without 50% nitrous oxide. Anesth Analg 1983; 62:449-512.
[21]Tomiei K, Tadayoshi K, Koji M, et al: Influence of Hemorrhage on Propofol Pseudo-Steady State Concentration. Anesthesiology 2002; 97:1156-61.
[22]Pascual JM, Runyon DE, Watson JC, Clifford CB, Dubick MA, Kramer GC. Resuscitation of hypovolemia in pigs using near saturated sodium chloride solution in dextran. Circ Shock 1993;40:115-24.
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[26]Cockshott ID, Douglas EJ, Plummer GF, Simons PJ: The pharmacokinetics of propofol in laboratory animals. Xenobiotica 1992; 22:369-75.
[27]Cockshott I, Briggs L, Douglas E, White M: Pharmacokinetics of propofol in female patients: Studies using single bolus injections. Br J Anesth 1987; 59:1103-10.
[28]Sebel PS, Lowdon JD: Propofl:A new intravenous anesthetic. Anesthesiology 1989;71:260-277.
[29]Hughes MA,Glass PSA,Jacobs JR. Context-sensitive half-time in multicompartment pharmacokinetic models for intravenous anaesthetic drugs. Anesthesiology 1992;76:334-341.
[30]Guyton AC: Textbook of Medical Physiology, 7th edition. Philadelphia, WB Saunders, 1986, pp 326-35.
[31]Rasmussen A, Skak C, Kristensen M, Ott P, Kirkegaard P, Secher NH: Preserved arterial flow secures hepatic oxygenation during haemorrhage in the pig. J Physiol 1999; 516:539-48.
[32]Martini L, Fini M, Giavaresi G, Faenza S, Petrini F, Giardino R: Haemodynamic and volumetric monitoring during haemorrhagic shock in swine. Resuscitation 2000; 51:69-76.
[33]Weiskopf RB, Bogertz MS, Roizen MF, Reid IA: Cardiovascular and metabolic sequelae of inducing anesthesia with ketamine or thiopental in hypovolemic swine. Anesthesiology 1984; 60:214-19.
[34]Johnson KB,Egan TD,Kem SE,et al:The influence of hemorrhagic shock on propofol:A pharmacokinetic and pharmacodynamic analysis. Anesthesiology 2003; 99:409-20.
[35]Ludbrook GL,Upton RN:A physiological model of induction of anaesthesia with propofol in sheep.2.Model analysis and implications for dose requirements. Br J Anaesth 1997;79:505-513.
[36]Myburgh JA, Upton RN, Grant C, Martinez A: Epinephrine, norepinephrine and dopamine infusions decrease propofol concentrations during continuous propofol infusion in an ovine model. Intensive Care Med 2001; 27:276-82.
[37]Upton RN, Ludbrook GL, Grant C, Martinez AM: Cardiac output is a determinant of the initial concentrations of propofol after short-infusion administration. Anesth Analg 1999; 89:545-52.
[38]Johansen J,Flaishon R, Sebel P.Esmlol reduces propofol requirement for skin incisin.Anesthesiology 1995;83:3A.
[39]Schuttler J,Ihmsen H.Population pharmacokinetics of propofol. Anesthesiology 2000;92:727-38.
[40]Kazama T, Ikeda K, Morita K, Ikeda T, Kikura M, Sato S: Relation between initial blood distribution volume and propofol induction dose requirement. Anesthesiology 2001; 94:205-10.
[41]Kuipers JA, Boer F, Olieman W, Burm AG, Bovill JG: First-pass lung uptake and pulmonary clearance of propofol: Assessment with a recirculatory indocyanine green pharmacokinetic model. Anesthesiology 1999; 91:1780-7.
[42]Lange H, Stephan H, Rieke H, Kellermann M, Sonntag H, Bircher J: Hepatic and extrahepatic disposition of propofol in patients undergoing coronary bypass surgery. Br J Anaesth 1990; 64:563-70.
[43]Mather LE, Selby DG, Runciman WB, McLean CF: Propofol: Assay and regional mass balance in the sheep. Xenobiotica 1989; 19:1337-47.
[44]Keiding S: Dynamic aspects of hepatic removal of circulating substances, Oxford Textbook of Clinical Hepatology. Edited by McIntyre N, Benhamou J, Bircher J, Rizzetto M, Rodes J. Oxford, Oxford Publishers, 199.1, pp78-87.
[45]Lindberg B: Liver circulation and metabolism in haemorrhagic shock: An experimental study with special reference to the effect of glucagon. Acta Chir Scand 1977; 476:1-18.
[46]DiPiro JT, Hooker KD, Sherman JC, Gaines MG, Wynn JJ: Effect of experimental hemorrhagic shock on hepatic drug elimination. Crit Care Med 1992; 20:810-5.
[47]Rasmussen A, Skak C, Kristensen M, Ott P, Kirkegaard P, Secher NH: Preserved arterial flow secures hepatic oxygenation during haemorrhage in the pig. J Physiol 1999; 516:539-48.
[48]Frink EJ Jr, Morgan SE, Coetzee A, Conzen PF, Brown BR Jr: The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs. Anesthesiology 1992; 76:85-90.
[49]Bernard JM, Doursout MF, Wouters P, Hartley CJ, Merin RG, Chelly JE: Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog. Anesthesiology 1992; 77:541-5.
[50]Lindberg B: Liver circulation and metabolism in haemorrhagic shock: An experimental study with special reference to the effect of glucagon. Acta Chir Scand 1977; 476:1-18.
[51]Adams P, Gelman S, Reves JG; Midazolam pharmacodynamics and pharmacokinetics during acute hypovolemia. Anesthesiology1985; 63: 140-6.
[52]Klockowski PM, Levy G; Kinetics of drug action in disease states. XXV: Effect of experimental hypovolemia on the pharmacodynamics and pharmacokinetics of desmethyldiazepam. J Pharmacol Exp Ther 1988; 245: 508-12.
[53]Dodd RY. The risk of transfusion-transmitted infection. N Engl J Med 1992;327:419-21.
[54]Blumberg N, Triulzi DJ, Heal JM. Transfusion-induced immunmodulation and its clinical consequences. Trans Med Rev 1990;24-35.
[55]Linden JV, Paul B, Dressier KP. A report of 304 transfusion errors in New York State. Transfusion 1992;32:601-6.
[56]Schriemer PA, Longnecker DE, Mintz PD. The possible immuno-suppressive effects of perioperative blood transfusion in cancer patients. Anesthesiology 1988;68:422-8.
[57]Surgenor DM, Wallace EL, Hao SH, et al. Collection and transfusion of blood in the United States. N Engl T Med 1990;322:1646-51.
[58]Toy PT, Strauss RG, Stehling LC, et al. Predeposited autologous blood for elective surgery: a national multicenter study. N EnglJ Med 1987;316:517-20.
[59]Consensus conference: Perioperative red blood cell transfusion. JAMA 1988;260:2700-3.
[60]Miller RD. Transfusion therapy. In: Miller RD, ed. Anesthesiology. New York: Churchill Li&gstone 1994:1619-46.
[61]Messmer KFW. Acceptable hematocrit levels in surgical patients. World JSurg 187; 11:41-6.
[62]Miller RD. Transfusion therapy. In: Miller RD, ed. Anesthesiology. New York: Churchill Li&gstone 1994:1619-46.
[63]Spahn DR, Leone BJ, Reves JG, et al. Cardiovascular and coronaryphysiology of acute isovolemic hemodilution: a review of nonoxygen-carrying and oxygen-carrying solutions. Anesth Analg 1994;78:1000-21.
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[65]Stehling LC, Zauder HL. Acute normovolemic hemodilution. Transfusion 1991 ;31:857-68.
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[70]Kumar R,Chakraborty I,Sehgal R. A Prospective Randomized Study Comparing Two Techniques of Perioperative Blood Conservation: Isovolemic Hemodilution and Hypervolemic Hemodilution. Anesth Analg 2002;95:1154-61.
[71]Mieke LL,Entholzner EK,Kling M,et al. Preoperative Acute Hypervolemic Hemodilution with Hydrovethylstarch: An Alternative to Acute normovolemic Hemodilution? Anesth Analg 1997;84:26-30.
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