Rabinovici R, Yue T L, Krausz M M, Sellers T S, Lynch K M, Feuerstein G
Department of Surgery, Jefferson Medical College, Philadelphia, Pennsylvania 19107.
Surg Gynecol Obstet. 1992 Oct;175(4):341-54.
Hypertonic saline solution (HTS) (7.5 percent sodium chloride [NaCl]) treatment (5 milliliters per kilogram) of rats subjected to uncontrolled hemorrhagic shock (n = 7) caused an initial partial recovery of blood pressure (+38 +/- 5 percent, p<0.05) and cardiac index (+48 +/- 6 percent, p<0.01) followed by increased bleeding (+53 +/- 5 percent versus rats treated with 0.9 percent NaCl, p<0.05), secondary shock (mean arterial pressure [MAP] 23 +/- 7 millimeters of mercury, p<0.01) and decreased survival (-54 +/- 15 minutes versus control, p<0.05). The increased blood loss resulted from: 1, increased vascular pressure and vasodilatation (total peripheral resistance index -27 +/- 5 percent, p<0.05), as initial bleeding occurred when MAP and cardiac index are increased compared with the control group (+88 +/- 10 percent, p<0.05 and +82 +/- 7 percent, p<0.01, respectively) and as the concomitant infusion of angiotensin II, a potent vasoconstrictor, delayed the HTS-induced bleeding (resumed at 60 minutes), and 2, a defect in platelet aggregation reflected by decreased adenosine diphosphate (ADP)-induced maximal aggregation (-79 percent versus rats treated with 0.9 percent NaCl, p<0.05) and increased EC50 of ADP (+159 percent, p<0.05). These hemodynamic and hematologic responses might be mediated at least in part by prostacyclin, a vasodilator and antiplatelet aggregator, as HTS-treated rats markedly elevated the 6-keto-PGF1 alpha per thromboxane B2 ratio (+140 +/- 12 percent, p<0.01) and pretreatment with indomethacin decreased blood loss and improved MAP and survival. These data point out potential untoward hemodynamic and hematologic consequences of HTS treatment in traumatic injury in which control of bleeding cannot be confirmed.
用高渗盐溶液（HTS）（7.5%氯化钠[NaCl]）以每千克5毫升的剂量治疗遭受非控制性失血性休克的大鼠（n = 7），血压（+38±5%，p<0.05）和心脏指数（+48±6%，p<0.01）最初会部分恢复，随后出血增加（与用0.9%氯化钠治疗的大鼠相比增加了+53±5%，p<0.05），出现继发性休克（平均动脉压[MAP]为23±7毫米汞柱，p<0.01），存活率降低（与对照组相比减少了-54±15分钟，p<0.05）。失血增加的原因如下：1. 血管压力增加和血管扩张（总外周阻力指数-27±5%，p<0.05），因为与对照组相比，当MAP和心脏指数增加时（分别为+88±10%，p<0.05和+82±7%，p<0.01）会发生初始出血，且同时输注血管紧张素II（一种强效血管收缩剂）会延迟HTS诱导的出血（60分钟时恢复）；2. 血小板聚集缺陷，表现为二磷酸腺苷（ADP）诱导的最大聚集降低（与用0.9%氯化钠治疗的大鼠相比降低了-79%，p<0.05）以及ADP的半数有效浓度（EC50）增加（+159%，p<0.05）。这些血流动力学和血液学反应可能至少部分由前列环素介导，前列环素是一种血管扩张剂和抗血小板聚集剂，因为用HTS治疗的大鼠显著提高了6-酮-前列腺素F1α与血栓素B2的比值（+140±12%，p<0.01），并且用吲哚美辛预处理可减少失血、改善MAP和存活率。这些数据指出了在无法确定出血是否得到控制的创伤性损伤中，HTS治疗可能产生的不良血流动力学和血液学后果。
