Heering P, Morgera S, Schmitz F J, Schmitz G, Willers R, Schultheiss H P, Strauer B E, Grabensee B
Department of Nephrology and Rheumatology, Heinrich-Heine-Universität,Düsseldorf, Germany.
Intensive Care Med. 1997 Mar;23(3):288-96. doi: 10.1007/s001340050330.
To determine whether continuous venovenous hemofiltration leads to extraction of tumor necrosis factor alpha (TNF alpha) and cytokines from the circulation of critically ill patients with sepsis and acute renal failure and to quantitate the clearance and the removal rate of these cytokines and their effect on serum cytokine concentrations.
Prospective, controlled study in patients with continuous venovenous hemofiltration (24 1/24 h) using a polysulphone membrane in patients with acute renal failure.
33 ventilated patients with acute renal failure of septic (n = 18) and cardiovascular origin (n = 15) were studied.
Hemodynamic monitoring and collection of blood and ultrafiltrate samples before and during the first 72 h of continuous hemofiltration.
Cardiovascular hemodynamics (Swan-Ganz catheter), Acute Physiology and Chronic Health Evaluation II score, creatinine, electrolytes, and blood urea nitrogen were recorded daily. Cytokines (TNF alpha, TNF alpha-RII, interleukin (IL) 1beta, IL1RA, IL2, IL2R, IL6, IL6R, IL8, IL10) were measured in prefilter blood and in ultrafiltrate immediately preceding and 12, 24, 48, and 72 h after initiating continuous venovenous hemofiltration (CVVH). Septic patients showed elevated cardiovascular values for cardiac output (7.2 +/- 2.1 l/min), cardiac index (4.2 +/- 1.3 l/min per m2), and stroke volume (67 +/- 23 ml) and reduced values for systemic vascular resistance (540 +/- 299 dyn x s x cm(-5)). All hemodynamic values normalized within the first 24 h after initiating CVVH treatment. TNF alpha was 1833 +/- 1217 pg/ml in septic patients and 42.9 +/- 6.3 pg/ml in nonseptic patients (p < 0.05) prior to CVVH. TNF alpha was detected in ultrafiltrate but did not decrease in blood during treatment with CVVH. There was no difference in IL 1beta between septic (3.8 +/- 1.9 pg/ml) and nonseptic patients (1.7 +/- 0.5 pg/ml). No significant elimination of cytokines was achieved in the present study by CVVH treatment.
These findings demonstrate that CVVH can remove TNF alpha and special cytokines from the circulation of critically ill patients. Cardiovascular hemodynamics seemed to improve in septic patients after induction of hemofiltration treatment, although there was no evidence that extracorporeal removal of cytokines achieved a reduction in blood levels. The study indicates that low volume continuous hemofiltration with polysulphone membranes in patients with acute renal failure is not able to induce significant removal of cytokines.
确定持续静静脉血液滤过是否能从患有脓毒症和急性肾衰竭的重症患者循环中清除肿瘤坏死因子α（TNFα）及细胞因子，并定量这些细胞因子的清除率和清除速度及其对血清细胞因子浓度的影响。
对使用聚砜膜进行持续静静脉血液滤过（24 小时持续滤过）的急性肾衰竭患者进行前瞻性对照研究。
研究了 33 例机械通气的急性肾衰竭患者，其中脓毒症导致的急性肾衰竭患者 18 例，心血管疾病导致的急性肾衰竭患者 15 例。
在持续血液滤过的前 72 小时内及期间进行血流动力学监测，并采集血液和超滤液样本。
每日记录心血管血流动力学指标（用 Swan - Ganz 导管测量）、急性生理与慢性健康状况评分 II、肌酐、电解质和血尿素氮。在开始持续静静脉血液滤过（CVVH）之前、开始后即刻、12、24、48 和 72 小时，分别测定滤器前血液和超滤液中的细胞因子（TNFα、TNFα - RII、白细胞介素（IL）1β、IL1RA、IL2、IL2R、IL6、IL6R、IL8、IL10）。脓毒症患者的心输出量（7.2±2.1 升/分钟）、心脏指数（4.2±1.3 升/分钟每平方米）和每搏输出量（67±23 毫升）的心血管数值升高，而全身血管阻力（540±299 达因×秒×厘米⁻⁵）数值降低。在开始 CVVH 治疗后的最初 24 小时内，所有血流动力学数值均恢复正常。CVVH 治疗前，脓毒症患者的 TNFα为 1833±1217 皮克/毫升，非脓毒症患者为 42.9±6.3 皮克/毫升（p<0.05）。在超滤液中检测到了 TNFα，但在 CVVH 治疗期间血液中的 TNFα并未降低。脓毒症患者（3.8±1.9 皮克/毫升）和非脓毒症患者（1.7±0.5 皮克/毫升）的 IL1β无差异。在本研究中，CVVH 治疗未实现细胞因子的显著清除。
这些发现表明 CVVH 可从重症患者循环中清除 TNFα和特定细胞因子。尽管没有证据表明体外清除细胞因子能使血液中细胞因子水平降低，但在脓毒症患者中，血液滤过治疗诱导后心血管血流动力学似乎有所改善。该研究表明，急性肾衰竭患者使用聚砜膜进行小容量持续血液滤过不能显著清除细胞因子。
