Kline J A, Gordon B E, Williams C, Blumenthal S, Watts J A, Diaz-Buxo J
Department Emergency Medicine Research, Cannon Research Center, Carolinas Medical Center, Charlotte, NC 28232, USA.
Crit Care Med. 1999 Mar;27(3):588-96. doi: 10.1097/00003246-199903000-00041.
This study was undertaken to test the hypothesis that hemodialysis with a large-pore membrane would improve heart function during acute endotoxin shock.
Large animal laboratory.
Eighteen mongrel dogs were instrumented to measure left ventricular maximum end-systolic elastance (left ventricular maximum elastance at end systole), cardiac output, circumflex artery blood flow, and myocardial mechanical efficiency (CO x MAP/MVO2, where CO is cardiac output, MAP is mean arterial pressure, and MVO2 is myocardial oxygen consumption). Plasma catecholamine concentrations were determined by high-performance liquid chromatography. Endotoxin shock was induced by infusing 5.0 microg/kg/min of Escherichia col 0127:B8 endotoxin in the portal vein for 60 mins, followed by 2.0 microg/kg/min of constant infusion. Control dogs (n = 6) received 4.0 mL/kg/min of saline; hemodialysis dogs (n = 6) underwent venovenous hemodialysis in 50-min intervals using a polysulfone filter (1.2 m2; mean pore size, 0.50 nm; blood flow rate, 400 mL/min; ultrafiltrate, "zero-balanced"); shams (n = 5) were treated identically to hemodialysis dogs, except that no convective dialysis was performed. A fourth group (n = 6) was treated with dopamine (5.0-7.0 microg/kg/min, optimal dose for contractile increase based on dose-response studies).
After 2 hrs of treatment, left ventricular maximum elastance at end systole increased and was unchanged in controls (30 +/- 5 mm Hg/mm) and shams (24 +/- 6 mm Hg/mm) compared with basal control. Hemodialysis treatment increased contractility (53 +/- 4 mm Hg/mm), as did dopamine treatment (54 +/- 7 mm Hg/mm). Endotoxin shock reduced mechanical efficiency to 45% of basal control; with hemodialysis treatment, left ventricular efficiency returned to 64% of basal control measurement, compared with 49% with dopamine treatment. During treatment, myocardial glucose uptake was increased with hemodialysis compared with other groups. No difference was observed among groups for left ventricular end-diastolic pressures or dimensions, or catecholamine concentrations.
Large-pore hemodialysis increased left ventricular contractility to a similar degree as dopamine and provided a marginal improvement in myocardial glucose uptake and mechanical efficiency.
本研究旨在验证以下假设,即使用大孔膜进行血液透析可改善急性内毒素休克期间的心脏功能。
大型动物实验室。
对18只杂种犬进行仪器安装,以测量左心室最大收缩末期弹性(收缩末期左心室最大弹性)、心输出量、回旋动脉血流量和心肌机械效率(心输出量×平均动脉压/心肌耗氧量,其中心输出量为心输出量,平均动脉压为平均动脉压,心肌耗氧量为心肌耗氧量)。通过高效液相色谱法测定血浆儿茶酚胺浓度。通过在门静脉中以5.0微克/千克/分钟的速度输注大肠杆菌0127:B8内毒素60分钟,然后以2.0微克/千克/分钟的速度持续输注来诱导内毒素休克。对照犬(n = 6)接受4.0毫升/千克/分钟的生理盐水;血液透析犬(n = 6)使用聚砜滤器(1.2平方米;平均孔径,0.50纳米;血流速度,400毫升/分钟;超滤液,“零平衡”)以50分钟的间隔进行静脉-静脉血液透析;假手术组(n = 5)的处理与血液透析犬相同,只是不进行对流透析。第四组(n = 6)用多巴胺(5.0 - 7.0微克/千克/分钟,根据剂量反应研究确定的增加收缩力的最佳剂量)进行治疗。
治疗2小时后,与基础对照相比,收缩末期左心室最大弹性增加,对照组(30±5毫米汞柱/毫米)和假手术组(24±6毫米汞柱/毫米)保持不变。血液透析治疗可增加收缩力(53±4毫米汞柱/毫米),多巴胺治疗也有同样效果(54±7毫米汞柱/毫米)。内毒素休克使机械效率降至基础对照的45%;血液透析治疗后,左心室效率恢复至基础对照测量值的64%,多巴胺治疗组为49%。在治疗期间,与其他组相比,血液透析可增加心肌葡萄糖摄取。各组在左心室舒张末期压力或尺寸或儿茶酚胺浓度方面未观察到差异。
大孔血液透析增加左心室收缩力的程度与多巴胺相似,并在心肌葡萄糖摄取和机械效率方面有轻微改善。