Brown J M, Grosso M A, Moore E E
Department of Surgery, Denver General Hospital, Colorado.
J Trauma. 1990 Jun;30(6):646-50; discussion 650-1.
Hypertonic saline with dextran (HSD) has been recently introduced for prehospital resuscitation of hemorrhagic shock, and is currently undergoing clinical investigation. To determine the effect of clinically relevant amounts of hypertonic saline (7.5% NaCl) and/or 6% dextran 70 on non-ischemic and post-ischemic hearts, we infused rat hearts (Langendorff, 20 minutes global ischemia, 37 degrees, 40 minutes' reperfusion) with: 1) 0.9% NaCl (control); 2) 7.5% NaCl/dextran; 3) 7.5% NaCl; or 4) dextran. We found that 7.5% NaCl alone or with dextran depressed ventricular function (developed pressure, DP; contractility, +dP/dt; and relaxation rate, -dP/dt) in non-ischemic hearts. In contrast, equimolar (2,400 mOsm) sucrose increased myocardial contractility (+dP/dt) of non-ischemic hearts. Coronary flow was unchanged by the addition of 7.5% NaCl, dextran, or sucrose. Treatment of ischemic hearts with 7.5% NaCl/dextran, dextran alone, or sucrose improved recovery of ventricular function compared to 0.9% or 7.5% NaCl. Furthermore, dextran (but not sucrose) with or without 7.5% NaCl reduced myocardial hydrogen peroxide (H2O2) levels during ischemia and reperfusion. We conclude that when given in clinically relevant amounts in the isolated rat heart: 1) 7.5% NaCl directly depresses myocardial function; 2) 7.5% NaCl alone does not improve post-ischemic ventricular function; 3) 7.5% NaCl with dextran or dextran alone improves post-ischemic ventricular function in part by reducing myocardial H2O2; and 4) sucrose equimolar to 7.5% HSD increases ventricular function in non-ischemic and post-ischemic hearts. This investigation suggests that the post-shock benefit of HSD is unrelated to direct myocardial effects of saline but is due in part to toxic oxygen metabolite scavenging by dextran.
高渗盐水与右旋糖酐（HSD）最近已被用于出血性休克的院前复苏，目前正在进行临床研究。为了确定临床相关剂量的高渗盐水（7.5%氯化钠）和/或6%右旋糖酐70对非缺血和缺血后心脏的影响，我们对大鼠心脏（Langendorff装置，20分钟全心缺血，37摄氏度，40分钟再灌注）进行灌注：1）0.9%氯化钠（对照组）；2）7.5%氯化钠/右旋糖酐；3）7.5%氯化钠；或4）右旋糖酐。我们发现，单独使用7.5%氯化钠或与右旋糖酐合用会降低非缺血心脏的心室功能（发展压力，DP；收缩性，+dP/dt；舒张速率，-dP/dt）。相比之下，等摩尔（2400毫渗量浓度）的蔗糖可增加非缺血心脏的心肌收缩性（+dP/dt）。添加7.5%氯化钠、右旋糖酐或蔗糖后冠状动脉血流量未发生变化。与0.9%或7.5%氯化钠相比，用7.5%氯化钠/右旋糖酐、单独使用右旋糖酐或蔗糖处理缺血心脏可改善心室功能的恢复。此外，右旋糖酐（但不是蔗糖）无论是否与7.5%氯化钠合用，均可降低缺血和再灌注期间心肌过氧化氢（H2O2）水平。我们得出结论，在离体大鼠心脏中给予临床相关剂量时：1）7.5%氯化钠直接抑制心肌功能；2）单独使用7.5%氯化钠不能改善缺血后心室功能；3）7.5%氯化钠与右旋糖酐合用或单独使用右旋糖酐可部分通过降低心肌H2O2来改善缺血后心室功能；4）与7.5% HSD等摩尔的蔗糖可增加非缺血和缺血后心脏的心室功能。这项研究表明，HSD休克后有益作用与盐水对心肌的直接作用无关，部分是由于右旋糖酐清除有毒氧代谢产物。
