七氟醚对缺血再灌注损伤所致内皮细胞糖蛋白被膜脱落的保护作用
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摘要
目的
讨论缺血再灌注损伤导致内皮细胞糖蛋白被膜脱落的程度及机理,七氟醚对内皮细胞糖蛋白被膜的保护作用及机理,以及不同处理模式对保护作用的影响。材料与方法
本研究采用豚鼠Langendorff离体心脏灌注模型,灌注压固定在70cmH20,灌注液选用改良Krebs-Henseleit液。分两部分进行。第一部分,健康雄性豚鼠42只,随机分为6组,A组为时间对照组,B组为七氟醚处理的时间对照组,c组为缺血再灌注损伤组,D组为用七氟醚预处理的缺血再灌注损伤组,E组为用七氟醚后处理的缺血再灌注损伤组,F组为用七氟醚预处理合并后处理的缺血再灌注损伤组。制备Langendorff离体心脏灌注模型。缺血再灌注损伤组接受20分钟全心停灌暖缺血(37℃),再灌注40分钟。七氟醚预处理组在20分钟暖缺血前接受15分钟2%七氟醚处理,七氟醚后处理组在20分钟暖缺血后在整个再灌注期间接受2%七氟醚处理。再灌注的后20分钟在K-H液中加入1%贺斯。观测指标包括渗出液,流出液的量,渗出液中组胺,肌酸激酶浓度,贺斯浓度,流出液中内皮细胞糖蛋白被膜主要成分-蛋白聚糖-1,硫酸化肝素,透明质酸浓度,乳酸,嘌呤,尿酸浓度。实验结束后,一些心脏被用于蛋白聚糖-1和硫酸化肝素的免疫组化染色,另一些心脏被用于电镜观察糖蛋白被膜的形态。第二部分,健康雄性豚鼠12只,随机分为2组,C组为缺血再灌注损伤组,F组为缺血预处理合并后处理的缺血再灌注损伤组。实验其他条件同前。观测指标为渗出液及流出液中组织蛋白酶B,类胰蛋白酶,不含凝血素的类胰蛋白酶浓度。
结果
1、缺血再灌注处理能引起渗出液增加,流出液减少,显著增加流出液中乳酸,嘌呤,尿酸浓度以及蛋白聚糖-1,硫酸化肝素,透明质酸浓度和渗出液中肌酸激酶,组胺及贺斯浓度。
2、免疫组化染色显示缺血再灌注处理使血管腔内的蛋白聚糖-1和硫酸化肝素染色呈阴性,镧染色电镜观察显示缺血再灌注处理使血管腔内的糖蛋白被膜几乎全部脱落。
3、应用七氟醚处理能减少渗出液以及渗出液中贺斯和肌酸激酶含量,但对渗出液中组胺含量没有明显影响。七氟醚处理能增加流出液的量,但对流出液中乳酸,嘌呤,尿酸浓度没有显著影响。七氟醚处理能降低流出液中糖蛋白被膜主要成分的浓度,使免疫组化染色蛋白聚糖-1和硫酸化肝素的染色增强,使电镜观察到的糖蛋白被膜脱落减少。
4、七氟醚还能使流出液中组织蛋白酶B浓度降低,对类胰蛋白酶和不含凝血素的类胰蛋白酶浓度无显著影响。
5、七氟醚处理的各组之间作用无显著差异。结论
1、缺血再灌注处理能使内皮细胞糖蛋白被膜脱落,增加内皮细胞通透性,并能显著增加心肌的氧化应激和无氧代谢,增加心肌细胞肌酸激酶和主细胞组胺的释放,降低心功能。
2、七氟醚预处理或后处理能够显著减少内皮细胞糖蛋白被膜的脱落,减少内皮细胞通透性从而降低渗出液中贺斯浓度,降低心肌细胞肌酸激酶的释放,改善再灌注后的心功能。但是对心肌的氧化应激和代谢无显著影响,也不能阻止主细胞释放组胺。在本实验的时间范围内,七氟醚预处理合并后处理不能获得保护作用的增强。
3、七氟醚对离体灌流心脏内皮细胞糖蛋白被膜保护作用的机制可能是结合在内皮细胞糖蛋白被膜或者未知蛋白酶的某些活性位点上,改变其结构和功能,从而抑制蛋白酶的释放或者降低蛋白酶的活性,减少酶解性内皮细胞糖蛋白被膜脱落。七氟醚对于主细胞脱颗粒没有显著抑制作用。
Aim
Healthy vascular endothelium is coated by the endothelial glycocalyx, diminution of which increases capillary permeability. The aims of this study is to evaluate the extent of glycocalyx shedding caused by ischemia-reperfusion injury and try to find its mechanism, to observe the effect of sevoflurane on shedding of endothelial glycocalyx caused by ischemia-reperfusion injury and try to find its mechanism, and to assess the effects of different models of sevoflurane treatment on endothelial glycocalyx.
Materials and methods
Isolated guinea pig hearts were perfused with modified Krebs-Henseleit (K-H) buffer, the perfusion pressure was maintained at 70 cmH20. The experiment was separated to two parts. The first part,42 healthy male guinea pigs were separated into 6 groups, isolated langendorff model was established on each of them. Group A was time-control group, group B was time-control group with sevoflurane treatment, group C was ischemia-reperfusion group, group D was ischemia-reperfusion injury group with sevoflurane pretreatment, group E was ischemia-reperfusion injury group with sevoflurane post-treatment, group F was ischemia-reperfusion group with sevoflurane pre-and post-treatment. Global warm ischemia (37℃) was induced for 20min in hearts of ischemia-reperfusion group, followed by 40min of reperfusion. In the last 20 min of reperfusion, hearts were perfused with Modified K-H buffer plus 1% of hydroxyethyl starch (130kd). Sevoflurane pretreatment was performed for 15min just before ischemia. Sevoflurane post-treatment was performed thought the whole reperfusion period. Coronary net fluid filtration was evaluated by measuring transudate formation on the epicedial surface. Hearts were perfusion fixed after the end of reperfusion to show the glycocalyx. Baseline measurements of coronary effluent and transudate were performed in the last 3 min before ischemia. Samples of effluent were also collected between minutes 0-5,5-10,10-20,35-40 after the onset of reperfusion. Transudate samples were collected over 5-min time intervals after start of reperfusion. Parameters including the concentration of shedding of components of glycocalyx (sydecan-1, heparan sulfate, and hyaluronan), lactate, purine, uric acid in effluent; the concentration of histamine, creatine kinase, hydroxyethyl starch in transudate. Electron microscopy of hearts to visible glycocalyx was performed and immunohistochemical characterization of hearts was conducted to gain insight into the composition of the glycocalyx. The second part, 12 healthy male guinea pigs were separated into 2 groups, isolated langendorff model was established as the first part. Group C was ischemia-reperfusion group, group S was ischemia-reperfusion group with sevoflurane pre-and post-treatment. Parameters including volume of transudate and effluent, concentrations of cathepsin-B, tryptase and tryptase without thrombin in transudate and effluent.
Results
1、Compared with time control group A and B, there was more transudate and less effluent in group C. Ischemia-reperfusion injury significantly increased the concentration of lactate, purine, uric acid, syndecan-1, heparan sulfate and hyluronic acid in effluent. Furthermore, concentration of histamine, creatin kinase, HES were significantly higher in group C.
2、Immunohistochemical staining showed that ischemia-reperfusion injury caused negative staining of syndecan-1 and heparin sulfate on endovascular surface, electron microscopy with lanthanum staining to visible endothelial glycocalyx showed severe shedding of glycocalyx on endovascular surface in ischemia-reperfusion injury group.
3、Application of sevoflurane reduced the volume of transudate, HES and creatine kinase levels in transudate but had no significant impact on the level of histamine. Sevoflurane increased the amount of effluent, but the lactic acid, purine, uric acid release in effluent was not significantly changed. Sevoflurane reduced the release of major components of glycocalyx in the effluent, so immunohistochemical staining of syndecan-1 and heparan sulfate enhanced, and electron microscopy showed that shedding of glycocalyx decreased.
4、Sevoflurane also reduced the release of cathepsin B in effluent, but had no significant effect on the release of the tryptase and tryptase without thrombin.
5、There is no significant difference among groups with sevoflurane pretreatment, posttreatment and pre-plus post-treatment.
Conclusions
1、Ischemia-reperfusion cause shedding of endothelial glycocalyx, thus increase the permeability of vascular. It also induce significant increases in myocardial oxidative stress, anaerobic metabolism, release of creatine kinase in myocardial cell and histamine in mast cell, thus reduce the cardiac function.
2、Sevoflurane significantly reduce shedding of the endothelial glycocalyx, thus reduce the permeability of small vessels and decrease the extravasation of HES, reduce the release of creatine kinase and improve post-reperfusion cardiac function. However, sevoflurane has no significant effect on oxidative stress and myocardial metabolism, nor prevente the release of histamine in mast cells. In this experiment time frame, compared to sevoflurane pretreatment, sevoflurane pre-plus post-treatment can not enhanced the protective effect.
3、The protective mechanism of sevoflurane on endothelial glycocalyx in this isolated guinea pig hearts maybe via binding of sevoflurane to the glycocalyx or to unknown proteinase(s) prevents enzymatic shedding during postischemia reperfusion of the heart, thus inhibited the release of protease or decrease the activity of protease. Sevoflurane has no significant effect on main cell degranulation.
讨论缺血再灌注损伤导致内皮细胞糖蛋白被膜脱落的程度及机理,七氟醚对内皮细胞糖蛋白被膜的保护作用及机理,以及不同处理模式对保护作用的影响。材料与方法
本研究采用豚鼠Langendorff离体心脏灌注模型,灌注压固定在70cmH20,灌注液选用改良Krebs-Henseleit液。分两部分进行。第一部分,健康雄性豚鼠42只,随机分为6组,A组为时间对照组,B组为七氟醚处理的时间对照组,c组为缺血再灌注损伤组,D组为用七氟醚预处理的缺血再灌注损伤组,E组为用七氟醚后处理的缺血再灌注损伤组,F组为用七氟醚预处理合并后处理的缺血再灌注损伤组。制备Langendorff离体心脏灌注模型。缺血再灌注损伤组接受20分钟全心停灌暖缺血(37℃),再灌注40分钟。七氟醚预处理组在20分钟暖缺血前接受15分钟2%七氟醚处理,七氟醚后处理组在20分钟暖缺血后在整个再灌注期间接受2%七氟醚处理。再灌注的后20分钟在K-H液中加入1%贺斯。观测指标包括渗出液,流出液的量,渗出液中组胺,肌酸激酶浓度,贺斯浓度,流出液中内皮细胞糖蛋白被膜主要成分-蛋白聚糖-1,硫酸化肝素,透明质酸浓度,乳酸,嘌呤,尿酸浓度。实验结束后,一些心脏被用于蛋白聚糖-1和硫酸化肝素的免疫组化染色,另一些心脏被用于电镜观察糖蛋白被膜的形态。第二部分,健康雄性豚鼠12只,随机分为2组,C组为缺血再灌注损伤组,F组为缺血预处理合并后处理的缺血再灌注损伤组。实验其他条件同前。观测指标为渗出液及流出液中组织蛋白酶B,类胰蛋白酶,不含凝血素的类胰蛋白酶浓度。
结果
1、缺血再灌注处理能引起渗出液增加,流出液减少,显著增加流出液中乳酸,嘌呤,尿酸浓度以及蛋白聚糖-1,硫酸化肝素,透明质酸浓度和渗出液中肌酸激酶,组胺及贺斯浓度。
2、免疫组化染色显示缺血再灌注处理使血管腔内的蛋白聚糖-1和硫酸化肝素染色呈阴性,镧染色电镜观察显示缺血再灌注处理使血管腔内的糖蛋白被膜几乎全部脱落。
3、应用七氟醚处理能减少渗出液以及渗出液中贺斯和肌酸激酶含量,但对渗出液中组胺含量没有明显影响。七氟醚处理能增加流出液的量,但对流出液中乳酸,嘌呤,尿酸浓度没有显著影响。七氟醚处理能降低流出液中糖蛋白被膜主要成分的浓度,使免疫组化染色蛋白聚糖-1和硫酸化肝素的染色增强,使电镜观察到的糖蛋白被膜脱落减少。
4、七氟醚还能使流出液中组织蛋白酶B浓度降低,对类胰蛋白酶和不含凝血素的类胰蛋白酶浓度无显著影响。
5、七氟醚处理的各组之间作用无显著差异。结论
1、缺血再灌注处理能使内皮细胞糖蛋白被膜脱落,增加内皮细胞通透性,并能显著增加心肌的氧化应激和无氧代谢,增加心肌细胞肌酸激酶和主细胞组胺的释放,降低心功能。
2、七氟醚预处理或后处理能够显著减少内皮细胞糖蛋白被膜的脱落,减少内皮细胞通透性从而降低渗出液中贺斯浓度,降低心肌细胞肌酸激酶的释放,改善再灌注后的心功能。但是对心肌的氧化应激和代谢无显著影响,也不能阻止主细胞释放组胺。在本实验的时间范围内,七氟醚预处理合并后处理不能获得保护作用的增强。
3、七氟醚对离体灌流心脏内皮细胞糖蛋白被膜保护作用的机制可能是结合在内皮细胞糖蛋白被膜或者未知蛋白酶的某些活性位点上,改变其结构和功能,从而抑制蛋白酶的释放或者降低蛋白酶的活性,减少酶解性内皮细胞糖蛋白被膜脱落。七氟醚对于主细胞脱颗粒没有显著抑制作用。
Aim
Healthy vascular endothelium is coated by the endothelial glycocalyx, diminution of which increases capillary permeability. The aims of this study is to evaluate the extent of glycocalyx shedding caused by ischemia-reperfusion injury and try to find its mechanism, to observe the effect of sevoflurane on shedding of endothelial glycocalyx caused by ischemia-reperfusion injury and try to find its mechanism, and to assess the effects of different models of sevoflurane treatment on endothelial glycocalyx.
Materials and methods
Isolated guinea pig hearts were perfused with modified Krebs-Henseleit (K-H) buffer, the perfusion pressure was maintained at 70 cmH20. The experiment was separated to two parts. The first part,42 healthy male guinea pigs were separated into 6 groups, isolated langendorff model was established on each of them. Group A was time-control group, group B was time-control group with sevoflurane treatment, group C was ischemia-reperfusion group, group D was ischemia-reperfusion injury group with sevoflurane pretreatment, group E was ischemia-reperfusion injury group with sevoflurane post-treatment, group F was ischemia-reperfusion group with sevoflurane pre-and post-treatment. Global warm ischemia (37℃) was induced for 20min in hearts of ischemia-reperfusion group, followed by 40min of reperfusion. In the last 20 min of reperfusion, hearts were perfused with Modified K-H buffer plus 1% of hydroxyethyl starch (130kd). Sevoflurane pretreatment was performed for 15min just before ischemia. Sevoflurane post-treatment was performed thought the whole reperfusion period. Coronary net fluid filtration was evaluated by measuring transudate formation on the epicedial surface. Hearts were perfusion fixed after the end of reperfusion to show the glycocalyx. Baseline measurements of coronary effluent and transudate were performed in the last 3 min before ischemia. Samples of effluent were also collected between minutes 0-5,5-10,10-20,35-40 after the onset of reperfusion. Transudate samples were collected over 5-min time intervals after start of reperfusion. Parameters including the concentration of shedding of components of glycocalyx (sydecan-1, heparan sulfate, and hyaluronan), lactate, purine, uric acid in effluent; the concentration of histamine, creatine kinase, hydroxyethyl starch in transudate. Electron microscopy of hearts to visible glycocalyx was performed and immunohistochemical characterization of hearts was conducted to gain insight into the composition of the glycocalyx. The second part, 12 healthy male guinea pigs were separated into 2 groups, isolated langendorff model was established as the first part. Group C was ischemia-reperfusion group, group S was ischemia-reperfusion group with sevoflurane pre-and post-treatment. Parameters including volume of transudate and effluent, concentrations of cathepsin-B, tryptase and tryptase without thrombin in transudate and effluent.
Results
1、Compared with time control group A and B, there was more transudate and less effluent in group C. Ischemia-reperfusion injury significantly increased the concentration of lactate, purine, uric acid, syndecan-1, heparan sulfate and hyluronic acid in effluent. Furthermore, concentration of histamine, creatin kinase, HES were significantly higher in group C.
2、Immunohistochemical staining showed that ischemia-reperfusion injury caused negative staining of syndecan-1 and heparin sulfate on endovascular surface, electron microscopy with lanthanum staining to visible endothelial glycocalyx showed severe shedding of glycocalyx on endovascular surface in ischemia-reperfusion injury group.
3、Application of sevoflurane reduced the volume of transudate, HES and creatine kinase levels in transudate but had no significant impact on the level of histamine. Sevoflurane increased the amount of effluent, but the lactic acid, purine, uric acid release in effluent was not significantly changed. Sevoflurane reduced the release of major components of glycocalyx in the effluent, so immunohistochemical staining of syndecan-1 and heparan sulfate enhanced, and electron microscopy showed that shedding of glycocalyx decreased.
4、Sevoflurane also reduced the release of cathepsin B in effluent, but had no significant effect on the release of the tryptase and tryptase without thrombin.
5、There is no significant difference among groups with sevoflurane pretreatment, posttreatment and pre-plus post-treatment.
Conclusions
1、Ischemia-reperfusion cause shedding of endothelial glycocalyx, thus increase the permeability of vascular. It also induce significant increases in myocardial oxidative stress, anaerobic metabolism, release of creatine kinase in myocardial cell and histamine in mast cell, thus reduce the cardiac function.
2、Sevoflurane significantly reduce shedding of the endothelial glycocalyx, thus reduce the permeability of small vessels and decrease the extravasation of HES, reduce the release of creatine kinase and improve post-reperfusion cardiac function. However, sevoflurane has no significant effect on oxidative stress and myocardial metabolism, nor prevente the release of histamine in mast cells. In this experiment time frame, compared to sevoflurane pretreatment, sevoflurane pre-plus post-treatment can not enhanced the protective effect.
3、The protective mechanism of sevoflurane on endothelial glycocalyx in this isolated guinea pig hearts maybe via binding of sevoflurane to the glycocalyx or to unknown proteinase(s) prevents enzymatic shedding during postischemia reperfusion of the heart, thus inhibited the release of protease or decrease the activity of protease. Sevoflurane has no significant effect on main cell degranulation.
引文
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[1]Brandstrup B, Tonnesen H, Beier-Holgersen R et al. Effects of intravenous fluid restriction on postoperative complications:comparison of two perioperative fluid regimens:a randomized assessor-blinded multicenter trial. Ann Surg.2003; 238: 641-648.
[2]Holte K, Kehlet H. Fluid therapy and surgical outcomes in elective surgery:a need for reassessment in fast-track surgery. J Am Coll Surg.2006; 202:971-989.
[3]Jacob M, Chappell D, Rehm M. Clinical update:perioperative fluid management. Lancet.2007; 369:1984-1986.
[4]Lobo DN, Bostock KA, Neal KR et al. Effect of salt and water balance on recovery of gastrointestinal function after elective colonic resection:a randomised controlled trial. Lancet.2002; 359:1812-1818.
[5]Nisanevich V, Felsenstein I, Almogy G et al. Effect of intraoperative fluid management on outcome after intraabdominal surgery. Anesthesiology.2005; 103: 25-32.
[6]Danielli JF. Capillary permeability and oedema in the perfused frog. J Physiol. 1940;98:109-129.
[7]Luft JH. Fine structures of capillary and endocapillary layer as revealed by ruthenium red. Fed Proc.1966; 25:1773-1783.
[8]Chappell D, Jacob M, Hofmann-Kiefer K et al. Hydrocortisone preserves the vascular barrier by protecting the endothelial glycocalyx. Anesthesiology.2007; 107:776-784.
[9]Rehm M, Zahler S, Lotsch M et al. Endothelial glycocalyx as an additional barrier determining extravasation of 6% hydroxyethyl starch or 5% albumin solutions in the coronary vascular bed. Anesthesiology.2004; 100:1211-1223.
[10]Nieuwdorp M, Meuwese MC, Vink H et al. The endothelial glycocalyx:a potential barrier between health and vascular disease. Curr Opin Lipidol.2005; 16:507-511
[11]Nieuwdorp M, Haeften TW van, Gouverneur MC et al. Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo. Diabetes.2006; 55:480-486.
[12]Klitzman B, Duling BR. Microvascular hematocrit and red cell flow in resting and contracting striated muscle. Am J Physiol.1979; 237:H481-H490.
[13]Fahraeus R, Lindquist T. The viscosity of the blood in narrow capillary tubes. Am J Physiol.1931;96:562-568.
[14]Jacob M, Bruegger D, Rehm M et al. Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability. Anesthesiology.2006; 104: 1223-1231.
[15]Rehm M, Bruegger D, Christ F et al. Shedding of the endothelial glycocalyx in patients undergoing major vascular surgery with global and regional ischemia. Circulation.2007; 116:1896-1906
[16]Potter DR, Damiano ER. The hydrodynamically relevant endothelial cell glycocalyx observed in vivo is absent in vitro. Circ Res.2008; 102:770-776.
[17]Reitsma S, Slaaf DW, Vink H et al. The endothelial glycocalyx:composition, functions and visualization. Pflugers Arch.2007; 454:345-359.
[18]Starling E. On the absorption of fluid from the connective tissue spaces. J Physiol (Lond).1896; 19:312-326.
[19]Levick JR. Revision of the Starling principle:new views of tissue fluid balance. J Physiol.2004; 557:704.
[20]Curry FE, Michel CC. A fiber matrix model of capillary permeability. Microvasc Res.1980; 20:96-99.
[21]Vink H, Duling BR. Capillary endothelial surface layer selectively reduces plasma solute distribution volume. Am J Physiol Heart Circ Physiol.2000; 278: H285-H289.
[22]Huxley VH, Curry FEAlbumin modulation of capillary permeability:test of an adsorption mechanism. Am J Physiol.1985; 248:H264-H273.
[23]Henry CB, Duran WN, DeFouw DO. Permselectivity of angiogenic microvessels following alteration of the endothelial fiber matrix by oligosaccharides. Microvasc Res.1997; 53:150-155.
[24]Hu X, Weinbaum S. A new view of Starling's hypothesis at the microstructural level. Microvasc Res.1999; 58:281-304.
[25]Adamson RH, Lenz JF, Zhang X et al. Oncotic pressures opposing filtration across non-fenestrated rat microvessels. J Physiol.2004; 557:889-907.
[26]Jacob M, Chappell D, Hofmann-Kiefer K et al. Determinants of insensible fluid loss. Perspiration, protein shift and endothelial glycocalyx. Anaesthesist 2007; 56: 747-764
[27]Bruegger D, Jacob M, Rehm M et al. Atrial natriuretic peptide induces shedding of endothelial glycocalyx in coronary vascular bed of guinea pig hearts. Am J Physiol Heart Circ Physiol,2005; 289:H1993-H1999.
[28]Rehm M, Orth V, Kreimeier U et al. Changes in intravascular volume during acute normovolemic hemodilution and intraoperative retransfusion in patients with radical hysterectomy. Anesthesiology.2000; 92:657-664.
[29]Rehm M, Haller M, Orth V et al. Changes in blood volume and hematocrit during acute preoperative volume loading with 5% albumin or 6% hetastarch solutions in patients before radical hysterectomy. Anesthesiology.2001; 95:849-856.
[30]Pries AR, Kuebler WM. Normal endothelium. Handb Exp Pharmacol.2006; 1: 1-40.
[31]Oliver MG, Specian RD, Perry MA, et al. Morphologic assessment of leukocyte-endothelial cell interactions in mesenteric venules subjected to ischemia and reperfusion. Inflammation.1991; 15:331-346.
[32]Nelson A, Berkestedt I, Schmidtchen A, et al. Increased levels of glycosaminoglycans during septic shock:relation to mortality and the antibacterial actions of plasma. Shock.2008; 30(6):623-7.
[33]Marechal X, Favory R, Joulin O et al. Endothelial glycocalyx damage during endotoxemia coincides with microcirculatory dysfunction and vascular oxidative stress.Shock.2008;29(5):572-6.
[34]Bernfield M, Gotte M, Park PW et al. Functions of cell surface heparan sulfate proteoglycans. Annu Rev Biochem.1999; 68:729-777.
[35]Vink H, Constantinescu AA, Spaan JA. Oxidized lipoproteins degrade the endothelial surface layer: implications for platelet-endothelial cell adhesion. Circulation.2000; 101:1500-1502
[36]Berg BM van den, Spaan JA, Rolf TM, Vink H. Atherogenic region and diet diminish glycocalyx dimension and increase intima-to-media ratios at murine carotid artery bifurcation. Am J Physiol Heart Circ Physiol.2006; 290: H915-H920
[37]Noble MI, Drake-Holland AJ, Vink H. Hypothesis:arterial glycocalyx dysfunction is the first step in the atherothrombotic process. QJM.2008; 101: 513-518.
[38]Algenstaedt P, Schaefer C, Biermann T et al. Microvascular alterations in diabetic mice correlate with level of hyperglycemia. Diabetes.2003; 52:542-549.
[39]Vlodavsky I, Ilan N, Nadir Y et al. Heparanase, heparin and the coagulation system in cancer progression. Thromb Res.2007; 120 [Suppl 2]:S112-S120.
[40]Shafat I, Zcharia E, Nisman B et al. An ELISA method for the detection and quantification of human heparanase. Biochem Biophys Res Commun.2006; 341: 958-963.
[41]Edovitsky E, Elkin M, Zcharia E et al. Heparanase gene silencing, tumor invasiveness, angiogenesis and metastasis. J Natl Cancer Inst.2004; 96: 1219-1230.
[42]Bruegger D, Rehm M, Jacob M et al. Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts. Crit Care.2008; 12:R73
[43]Constantinescu AA, Vink H, Spaan JA. Endothelial cell glycocalyx modulates immobilization of leukocytes at the endothelial surface. Arterioscler Thromb Vasc Biol.2003; 23:1541-1547
[1]Chan ST, Kapadia CR, Johnson AW, Radcliffe AG, Dudley HA:Extracellular fluid volume expansion and third space sequestration at the site of small bowel anastomoses. Br J Surg 1983; 70:36-9
[2]Arieff AI:Fatal postoperative pulmonary edema: Pathogenesis and literature review. Chest 1999; 115:1371-7
[3]Klein HG, Spahn DR, Carson JL: Red blood cell transfusion in clinical practice. Lancet 2007; 370:415-26
[4]Brun JF, Bouchahda C, Chaze D, Benhaddad AA, Micallef JP, Mercier J:The paradox of hematocrit in exercise physiology: Which is the "normal" range from an hemorheologist's viewpoint? Clin Hemorheol Microcirc 2000; 22:287-303
[5]Kozek-Langenecker SA:Effects of hydroxyethyl starch solutions on hemostasis. Anesthesiology 2005; 103:654-60
[6]Kaye AD, Kucera AJ:Fluid and electrolyte physiology, Anesthesia,6th edition. Edited by Miller RD. Philadelphia, Churchill Livingstone,2005,
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[8]Campbell IT, Baxter JN, Tweedie IE, Taylor GT, Keens SJ:IV fluids during surgery. Br J Anaesth 1990; 65:726-9
[9]Richer M, Robert S, Lebel M:Renal hemodynamics during norepinephrine and low-dose dopamine infusions in man. Crit Care Med 1996; 24:1150-6
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[15]Rehm M, Orth VH, Kreimeier U, Thiel M, Mayer S, Brechtelsbauer H, Finsterer U:Changes in blood volume during acute normovolemic hemodilution with 5% albumin or 6% hydroxyethylstarch and intraoperative retransfusion. Anaesthesist 2001; 50:569-79
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[27]Hu X, Adamson RH, Liu B, Curry FE, Weinbaum S:Starling forces that oppose filtration after tissue oncotic pressure is increased. Am J Physiol Heart Circ Physiol 2000; 279:H1724-36
[28]Constantinescu AA, Vink H, Spaan JA:Endothelial cell glycocalyx modulates immobilization of leukocytes at the endothelial surface. Arterioscler Thromb Vasc Biol 2003; 23:1541-7
[29]Kamp-Jensen M, Olesen KL, Bach V, Schutten HJ, Engquist A:Changes in serum electrolyte and atrial natriuretic peptide concentrations, acid-base and haemodynamic status after rapid infusion of isotonic saline and Ringer lactate solution in healthy volunteers. Br J Anaesth 1990; 64:606-10
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[36]Rehm M, Bruegger D, Christ F et al. Shedding of the endothelial glycocalyx in patients undergoing major vascular surgery with global and regional ischemia. Circulation.2007; 116:1896-1906
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[2]Mulivor AW, Lipowsky HH. Inflammation-and ischemia-induced shedding of venular glycocalyx. Am J Physiol Heart Circ Physiol.2004 May;286(5): H1672-80.
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[7]Vink H, Constantinescu AA, Spaan JA. Oxidized lipoproteins degrade the endothelial surface layer: implications for platelet-endothelial cell adhesion. Circulation.2000;101:1500-1502.
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[14]Adamson RH, Lenz JF, Zhang X, Adamson GN, Weinbaum S, Curry FE: Oncotic pressures opposing filtration across non-fenestrated rat microvessels. J Physiol 2004; 557:889-907
[15]Hu X, Adamson RH, Liu B, Curry FE, Weinbaum S:Starling forces that oppose filtration after tissue oncotic pressure is increased. Am J Physiol Heart Circ Physiol 2000; 279:H1724-36
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[17]Chappell D, Jacob M, Hofmann-Kiefer K, et al. Hydrocortisone preserves the vascular barrier by protecting the endothelial glycocalyx. Anesthesiology 2007; 107:776-84
[18]Chappell D, Jacob M, Hofmann-Kiefer K, et al. Antithrombin reduces shedding of endothelial glycocalyx following ischaemia/reperfusion. Cardiovasc Res 2009; 83:388-96
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[26]Chappell D, Jacob M, Becker BF, et al. Expedition glycocalyx. A newly discovered "Great Barrier Reef". Anaesthesist.2008; 57:959-69. German.
[1]Brandstrup B, Tonnesen H, Beier-Holgersen R et al. Effects of intravenous fluid restriction on postoperative complications:comparison of two perioperative fluid regimens:a randomized assessor-blinded multicenter trial. Ann Surg.2003; 238: 641-648.
[2]Holte K, Kehlet H. Fluid therapy and surgical outcomes in elective surgery:a need for reassessment in fast-track surgery. J Am Coll Surg.2006; 202:971-989.
[3]Jacob M, Chappell D, Rehm M. Clinical update:perioperative fluid management. Lancet.2007; 369:1984-1986.
[4]Lobo DN, Bostock KA, Neal KR et al. Effect of salt and water balance on recovery of gastrointestinal function after elective colonic resection:a randomised controlled trial. Lancet.2002; 359:1812-1818.
[5]Nisanevich V, Felsenstein I, Almogy G et al. Effect of intraoperative fluid management on outcome after intraabdominal surgery. Anesthesiology.2005; 103: 25-32.
[6]Danielli JF. Capillary permeability and oedema in the perfused frog. J Physiol. 1940;98:109-129.
[7]Luft JH. Fine structures of capillary and endocapillary layer as revealed by ruthenium red. Fed Proc.1966; 25:1773-1783.
[8]Chappell D, Jacob M, Hofmann-Kiefer K et al. Hydrocortisone preserves the vascular barrier by protecting the endothelial glycocalyx. Anesthesiology.2007; 107:776-784.
[9]Rehm M, Zahler S, Lotsch M et al. Endothelial glycocalyx as an additional barrier determining extravasation of 6% hydroxyethyl starch or 5% albumin solutions in the coronary vascular bed. Anesthesiology.2004; 100:1211-1223.
[10]Nieuwdorp M, Meuwese MC, Vink H et al. The endothelial glycocalyx:a potential barrier between health and vascular disease. Curr Opin Lipidol.2005; 16:507-511
[11]Nieuwdorp M, Haeften TW van, Gouverneur MC et al. Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo. Diabetes.2006; 55:480-486.
[12]Klitzman B, Duling BR. Microvascular hematocrit and red cell flow in resting and contracting striated muscle. Am J Physiol.1979; 237:H481-H490.
[13]Fahraeus R, Lindquist T. The viscosity of the blood in narrow capillary tubes. Am J Physiol.1931;96:562-568.
[14]Jacob M, Bruegger D, Rehm M et al. Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability. Anesthesiology.2006; 104: 1223-1231.
[15]Rehm M, Bruegger D, Christ F et al. Shedding of the endothelial glycocalyx in patients undergoing major vascular surgery with global and regional ischemia. Circulation.2007; 116:1896-1906
[16]Potter DR, Damiano ER. The hydrodynamically relevant endothelial cell glycocalyx observed in vivo is absent in vitro. Circ Res.2008; 102:770-776.
[17]Reitsma S, Slaaf DW, Vink H et al. The endothelial glycocalyx:composition, functions and visualization. Pflugers Arch.2007; 454:345-359.
[18]Starling E. On the absorption of fluid from the connective tissue spaces. J Physiol (Lond).1896; 19:312-326.
[19]Levick JR. Revision of the Starling principle:new views of tissue fluid balance. J Physiol.2004; 557:704.
[20]Curry FE, Michel CC. A fiber matrix model of capillary permeability. Microvasc Res.1980; 20:96-99.
[21]Vink H, Duling BR. Capillary endothelial surface layer selectively reduces plasma solute distribution volume. Am J Physiol Heart Circ Physiol.2000; 278: H285-H289.
[22]Huxley VH, Curry FEAlbumin modulation of capillary permeability:test of an adsorption mechanism. Am J Physiol.1985; 248:H264-H273.
[23]Henry CB, Duran WN, DeFouw DO. Permselectivity of angiogenic microvessels following alteration of the endothelial fiber matrix by oligosaccharides. Microvasc Res.1997; 53:150-155.
[24]Hu X, Weinbaum S. A new view of Starling's hypothesis at the microstructural level. Microvasc Res.1999; 58:281-304.
[25]Adamson RH, Lenz JF, Zhang X et al. Oncotic pressures opposing filtration across non-fenestrated rat microvessels. J Physiol.2004; 557:889-907.
[26]Jacob M, Chappell D, Hofmann-Kiefer K et al. Determinants of insensible fluid loss. Perspiration, protein shift and endothelial glycocalyx. Anaesthesist 2007; 56: 747-764
[27]Bruegger D, Jacob M, Rehm M et al. Atrial natriuretic peptide induces shedding of endothelial glycocalyx in coronary vascular bed of guinea pig hearts. Am J Physiol Heart Circ Physiol,2005; 289:H1993-H1999.
[28]Rehm M, Orth V, Kreimeier U et al. Changes in intravascular volume during acute normovolemic hemodilution and intraoperative retransfusion in patients with radical hysterectomy. Anesthesiology.2000; 92:657-664.
[29]Rehm M, Haller M, Orth V et al. Changes in blood volume and hematocrit during acute preoperative volume loading with 5% albumin or 6% hetastarch solutions in patients before radical hysterectomy. Anesthesiology.2001; 95:849-856.
[30]Pries AR, Kuebler WM. Normal endothelium. Handb Exp Pharmacol.2006; 1: 1-40.
[31]Oliver MG, Specian RD, Perry MA, et al. Morphologic assessment of leukocyte-endothelial cell interactions in mesenteric venules subjected to ischemia and reperfusion. Inflammation.1991; 15:331-346.
[32]Nelson A, Berkestedt I, Schmidtchen A, et al. Increased levels of glycosaminoglycans during septic shock:relation to mortality and the antibacterial actions of plasma. Shock.2008; 30(6):623-7.
[33]Marechal X, Favory R, Joulin O et al. Endothelial glycocalyx damage during endotoxemia coincides with microcirculatory dysfunction and vascular oxidative stress.Shock.2008;29(5):572-6.
[34]Bernfield M, Gotte M, Park PW et al. Functions of cell surface heparan sulfate proteoglycans. Annu Rev Biochem.1999; 68:729-777.
[35]Vink H, Constantinescu AA, Spaan JA. Oxidized lipoproteins degrade the endothelial surface layer: implications for platelet-endothelial cell adhesion. Circulation.2000; 101:1500-1502
[36]Berg BM van den, Spaan JA, Rolf TM, Vink H. Atherogenic region and diet diminish glycocalyx dimension and increase intima-to-media ratios at murine carotid artery bifurcation. Am J Physiol Heart Circ Physiol.2006; 290: H915-H920
[37]Noble MI, Drake-Holland AJ, Vink H. Hypothesis:arterial glycocalyx dysfunction is the first step in the atherothrombotic process. QJM.2008; 101: 513-518.
[38]Algenstaedt P, Schaefer C, Biermann T et al. Microvascular alterations in diabetic mice correlate with level of hyperglycemia. Diabetes.2003; 52:542-549.
[39]Vlodavsky I, Ilan N, Nadir Y et al. Heparanase, heparin and the coagulation system in cancer progression. Thromb Res.2007; 120 [Suppl 2]:S112-S120.
[40]Shafat I, Zcharia E, Nisman B et al. An ELISA method for the detection and quantification of human heparanase. Biochem Biophys Res Commun.2006; 341: 958-963.
[41]Edovitsky E, Elkin M, Zcharia E et al. Heparanase gene silencing, tumor invasiveness, angiogenesis and metastasis. J Natl Cancer Inst.2004; 96: 1219-1230.
[42]Bruegger D, Rehm M, Jacob M et al. Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts. Crit Care.2008; 12:R73
[43]Constantinescu AA, Vink H, Spaan JA. Endothelial cell glycocalyx modulates immobilization of leukocytes at the endothelial surface. Arterioscler Thromb Vasc Biol.2003; 23:1541-1547
[1]Chan ST, Kapadia CR, Johnson AW, Radcliffe AG, Dudley HA:Extracellular fluid volume expansion and third space sequestration at the site of small bowel anastomoses. Br J Surg 1983; 70:36-9
[2]Arieff AI:Fatal postoperative pulmonary edema: Pathogenesis and literature review. Chest 1999; 115:1371-7
[3]Klein HG, Spahn DR, Carson JL: Red blood cell transfusion in clinical practice. Lancet 2007; 370:415-26
[4]Brun JF, Bouchahda C, Chaze D, Benhaddad AA, Micallef JP, Mercier J:The paradox of hematocrit in exercise physiology: Which is the "normal" range from an hemorheologist's viewpoint? Clin Hemorheol Microcirc 2000; 22:287-303
[5]Kozek-Langenecker SA:Effects of hydroxyethyl starch solutions on hemostasis. Anesthesiology 2005; 103:654-60
[6]Kaye AD, Kucera AJ:Fluid and electrolyte physiology, Anesthesia,6th edition. Edited by Miller RD. Philadelphia, Churchill Livingstone,2005,
[7]Maharaj CH, Kallam SR, Malik A, Hassett P, Grady D, Laffey JG:Preoperative intravenous fluid therapy decreases postoperative nausea and pain in high risk patients. Anesth Analg 2005; 100:675-82
[8]Campbell IT, Baxter JN, Tweedie IE, Taylor GT, Keens SJ:IV fluids during surgery. Br J Anaesth 1990; 65:726-9
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