Bickell W H, Bruttig S P, Millnamow G A, O'Benar J, Wade C E
Division of Military Trauma Research, Letterman Army Institute of Research, Presidio of San Francisco, California.
Ann Emerg Med. 1992 Sep;21(9):1077-85. doi: 10.1016/s0196-0644(05)80648-1.
We tested the hypothesis that following aortotomy, administration of hypertonic saline/dextran increases hemorrhage and mortality. We also compared hypertonic saline/dextran with the standard therapy of attempting to replace three times the amount of lost blood with lactated Ringer's solution.
In this model of uncontrolled arterial hemorrhage resulting from aortotomy, 24 anesthetized Yorkshire swine underwent splenectomy, stainless steel wire placement in the infrarenal aorta, and instrumentation with Swan-Ganz and carotid artery catheters. The wire was pulled, producing a 5-mm aortotomy and spontaneous intraperitoneal hemorrhage.
The animals were randomly assigned to one of three study groups: control; hypertonic saline/dextran group in which six minutes after aortotomy a 4-mL/kg mixture of IV 7.5% NaCl and 6% Dextran-70 was given over one minute; or lactated Ringer's group in which six minutes after aortotomy 80 mL/kg IV lactated Ringer's was given over nine minutes.
The volume of hemorrhage and the mortality rate in hypertonic saline/dextran-treated animals were significantly greater than in the nonresuscitated controls (1,340 +/- 230 mL versus 783 +/- 85 mL and five of eight versus zero of eight, respectively; P less than .05). Although the mortality rate in the lactated Ringer's group was not significantly different from the hypertonic saline/dextran group, survival time was significantly shorter than in the hypertonic saline/dextran group.
In this model of uncontrolled hemorrhage, immediate IV administration of hypertonic saline/dextran significantly increased hemorrhage volume and mortality. However, the accentuation of hemorrhage and reduction in survival were not as great as that produced by the standard practice of attempting to replace the lost blood with three times that volume of lactated Ringer's.
我们检验了以下假设,即主动脉切开术后给予高渗盐水/右旋糖酐会增加出血量和死亡率。我们还将高渗盐水/右旋糖酐与试图用三倍失血量的乳酸林格氏液进行替代的标准疗法进行了比较。
在这个由主动脉切开术导致的未控制动脉出血模型中,24只麻醉的约克郡猪接受了脾切除术、在肾下主动脉放置不锈钢丝以及用Swan-Ganz导管和颈动脉导管进行仪器植入。拔出钢丝,造成5毫米的主动脉切开术和自发性腹腔内出血。
动物被随机分配到三个研究组之一:对照组;高渗盐水/右旋糖酐组,在主动脉切开术后6分钟,静脉注射4毫升/千克的7.5%氯化钠和6%右旋糖酐-70混合液,持续1分钟;或乳酸林格氏液组,在主动脉切开术后6分钟,静脉注射80毫升/千克的乳酸林格氏液,持续9分钟。
高渗盐水/右旋糖酐治疗的动物的出血量和死亡率显著高于未复苏的对照组(分别为1340±230毫升对783±85毫升,8只中有5只对8只中有0只;P<0.05)。虽然乳酸林格氏液组的死亡率与高渗盐水/右旋糖酐组没有显著差异,但生存时间显著短于高渗盐水/右旋糖酐组。
在这个未控制出血的模型中,立即静脉注射高渗盐水/右旋糖酐显著增加了出血量和死亡率。然而,出血的加重和生存时间的缩短不如试图用三倍失血量的乳酸林格氏液进行替代的标准做法那么严重。