Welte M, Goresch T, Frey L, Holzer K, Zwissler B, Messmer K
Department of Anesthesiology, Klinikum Grosshadern, University of Munich, Germany.
Anesth Analg. 1995 Jun;80(6):1099-107. doi: 10.1097/00000539-199506000-00006.
Small volumes of hypertonic saline dextran (10% of shed blood volume [SBV] restore cardiac output (CO) and increase arterial pressure in hemorrhagic shock. Besides rapid expansion of plasma volume, a positive inotropic effect has been proposed as an additional mechanism for the immediate onset of the cardiovascular response. This study compares the effects of 7.2% saline/10% dextran 60 (HSDex, n = 8) and normal saline (NS; n = 6) on central hemodynamics and cardiac contractility assessed by end-systolic elastance (Ees; conductance technique) and segmental preload recruitable stroke work (sPRSW; sonomicrometry). In anesthetized open chest pigs (28 +/- 1 kg, mean +/- SEM) shock was induced by blood withdrawal (40% of blood volume) to maintain mean arterial pressure (MAP) at 45 mm Hg for 75 min. Resuscitation was started by bolus infusion (2 min) of either HSDex (10% of SBV) or the identical sodium load of NS (80% of SBV); 30 min later both groups received 6% dextran (10% of SBV). Hemorrhagic shock reduced CO (-45%) and left ventricular end-diastolic volume (Ved; -70%) while Ees increased (NS:2.2 +/- 0.4 to 7.5 +/- 1.8 mm Hg/mL, P < 0.05; HSDex: 1.9 +/- 0.2 to 9.1 +/- 2.6 mm Hg/mL, P = 0.085). Within 5 min after infusion of either solution CO returned to baseline values and MAP (NS +55%, HSDex +64%) and Ved (+100%) increased. Neither HSDex nor NS increased Ees above shock levels (NS, 8.7 +/- 4.9 mm Hg/mL; HSDex, 7.3 +/- 2.6 mm Hg/mL) and no group differences occurred in other measurements of contractility (dP/dt40,sPRSW). Plasma osmolality increased to 328 +/- 3 mOsmol/kg with HSDex.(ABSTRACT TRUNCATED AT 250 WORDS)
小剂量高渗盐水右旋糖酐（失血量的10%）可恢复失血性休克患者的心输出量（CO）并升高动脉压。除了能快速扩充血浆容量外，正性肌力作用被认为是心血管反应迅速起效的另一种机制。本研究比较了7.2%盐水/10%右旋糖酐60（高渗盐水右旋糖酐，n = 8）和生理盐水（NS；n = 6）对通过收缩末期弹性（Ees；电导技术）和节段性可募集前负荷搏功（sPRSW；超声测量法）评估的中心血流动力学和心脏收缩性的影响。在麻醉开胸猪（28±1 kg，均值±标准误）中，通过放血（血容量的40%）诱导休克，将平均动脉压（MAP）维持在45 mmHg 75分钟。通过推注输注（2分钟）高渗盐水右旋糖酐（失血量的'10%）或相同钠负荷的生理盐水（失血量的80%）开始复苏；30分钟后两组均接受6%右旋糖酐（失血量的10%）。失血性休克使CO降低（-45%），左心室舒张末期容积（Ved；-70%）降低，而Ees升高（NS：2.2±0.4至7.5±1.8 mmHg/mL，P<0.05；高渗盐水右旋糖酐：1.9±0.2至9.1±2.6 mmHg/mL，P = 0.085）。输注任何一种溶液后5分钟内，CO恢复至基线值，MAP（NS升高55%，高渗盐水右旋糖酐升高64%）和Ved（升高100%）增加。高渗盐水右旋糖酐和生理盐水均未使Ees升高超过休克水平（NS为8.7±4.9 mmHg/mL；高渗盐水右旋糖酐为7.3±2.6 mmHg/mL），且在其他收缩性测量指标（dp/dt40，sPRSW）上两组无差异。高渗盐水右旋糖酐使血浆渗透压升至328±3 mOsmol/kg。（摘要截断于250字）
