Journal
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Volume 161, Issue 5, Pages 1429-1436Publisher
AMER THORACIC SOC
DOI: 10.1164/ajrccm.161.5.9809127
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High volume hemofiltration (HVHF) (200 ml/kg/h) improves hemodynamics in experimental septic shock but is difficult to apply clinically. Accordingly, we studied whether less intensive HVHF (80 ml/kg/h) can still improve hemodynamics in experimental septic shock. We also investigated its effect on the serum concentrations of several inflammatory mediators, including endothelin (ET-1), endotoxin (LPS), tumor necrosis factor-alpha (TNF-alpha), and 6-keto prostaglandin F-1 alpha (6-kepto PGF(1 alpha)). Sixteen anesthetized dogs were connected to a continuous veno-venous hemofiltration (CVVH) (filtration: 80 ml/kg/h) or sham circuit and endotoxin (0.5 mg/kg) was infused intravenously over 5 min. Hemodynamic variables were measured at baseline and at 15, 45, 90, and 180 min. The major hemodynamic finding was that endotoxin-induced hypotension was significantly attenuated by intensive CVVH (p < 0.04). Changes in cardiac output and right ventricular ejection fraction were equal in both groups. ET-1 levels, but not LPS, TNF-alpha, or 6-keto PGF(1 alpha), were lower during CVVH (p = 0.042). Endotoxin or TNF-a were not found in the ultrafiltrate. Median clearances of ET-1 and 6-keto PCF1 alpha during intensive CVVH were 8.8 and 25.9 ml/m, respectively. We conclude that intensive CWH attenuates the early component of endotoxin-induced hypotension and reduces serum concentrations of endothelin-l. The effect of CWH on blood pressure is not explained by convective clearance of the mediators in question.
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