Rehm Markus, Zahler Stefan, Lötsch Michael, Welsch Ulrich, Conzen Peter, Jacob Matthias, Becker Bernhard Friedrich
Klinik für Anästhesiologie, Ludwig-Maximilians-Universität München, Klinikum Grosshadern, Marchioninistr. 15, D-81377 Munich, Germany.
Anesthesiology. 2004 May;100(5):1211-23. doi: 10.1097/00000542-200405000-00025.
The impact on the endothelial glycocalyx for the extravasation of colloidal infusion solutions has not been investigated sufficiently.
Isolated guinea pig hearts were perfused with Krebs-Henseleit buffer in a Langendorff mode. Solutions of 0.9% saline, 5% albumin (70 kd), or 6% hydroxyethyl starch (200 kd) were infused into the coronary system for 20 min at a rate of one third of the coronary flow, also during reperfusion after 15 min of ischemia, and after enzymatic digestion of the endothelial glycocalyx by heparinase. Net coronary fluid filtration was assessed directly by measuring the formation of transudate on the epicardial surface, and solute extravasation was assessed by measuring albumin and hydroxyethyl starch in the coronary effluent and transudate. Hearts were perfusion fixed to visualize the endothelial glycocalyx using transmission electron microscopy.
Only infusion of hydroxyethyl starch, not infusion of albumin, significantly decreased net coronary fluid filtration. Heparinase application without ischemia increased coronary leak by 25% but did not accelerate the passage of colloids. Ischemia alone did not alter permeability. However, there was a large (approximately +200%), transient (approximately 4 min) increase in permeability for water, albumin, and hydroxyethyl starch after ischemia with heparinase application. Also, histamine (10 m) only increased permeability after pretreatment of the hearts with heparinase. The thickness of the glycocalyx after colloid administration was 0.2-0.3 microm. No glycocalyx could be detected after application of heparinase.
The endothelial glycocalyx acts as a competent barrier for water and colloids. Only after its destruction do changes in endothelial morphology (postischemic reperfusion or histamine application) become effective determinants of coronary extravasation.
胶体输注溶液外渗对内皮糖萼的影响尚未得到充分研究。
采用Langendorff模式,用Krebs-Henseleit缓冲液灌注离体豚鼠心脏。将0.9%生理盐水、5%白蛋白(70kd)或6%羟乙基淀粉(200kd)溶液以冠状动脉血流量的三分之一的速率注入冠状动脉系统20分钟,在缺血15分钟后的再灌注期间以及用肝素酶对内皮糖萼进行酶消化后也进行注入。通过测量心外膜表面渗出液的形成直接评估冠状动脉净液体滤过,并通过测量冠状动脉流出液和渗出液中的白蛋白和羟乙基淀粉来评估溶质外渗。对心脏进行灌注固定,使用透射电子显微镜观察内皮糖萼。
只有输注羟乙基淀粉,而不是输注白蛋白,能显著降低冠状动脉净液体滤过。在没有缺血的情况下应用肝素酶可使冠状动脉渗漏增加25%,但并未加速胶体的通过。单独缺血不会改变通透性。然而,在缺血并应用肝素酶后,水、白蛋白和羟乙基淀粉的通透性有一个大幅(约+200%)、短暂(约4分钟)的增加。此外,组胺(10μM)仅在心脏用肝素酶预处理后才增加通透性。给予胶体后糖萼的厚度为0.2 - 0.3微米。应用肝素酶后未检测到糖萼。
内皮糖萼对水和胶体起着有效的屏障作用。只有在其被破坏后,内皮形态的改变(缺血后再灌注或应用组胺)才成为冠状动脉外渗的有效决定因素。