The effect of intensive plasma water exchange by hemofiltration on hemodynamics and soluble mediators in canine endotoxemia.
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(1alpha) (6-kepto PGF(1alpha)). 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(1alpha), were lower during CVVH (p = 0.042). Endotoxin or TNF-alpha were not found in the ultrafiltrate. Median clearances of ET-1 and 6-keto PGF(1alpha) during intensive CVVH were 8.8 and 25.9 ml/m, respectively. We conclude that intensive CVVH attenuates the early component of endotoxin-induced hypotension and reduces serum concentrations of endothelin-1. The effect of CVVH on blood pressure is not explained by convective clearance of the mediators in question.
Bellomo
R
R
Department of Anesthesiology, University of Pittsburgh Medical Centre, Pittsburgh, Pennsylvania, USA.
Kellum
J A
JA
Gandhi
C R
CR
Pinsky
M R
MR
Ondulik
B
B
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D019332:Endothelin-1 / Q000097:blood; D019446:Endotoxemia / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics; D006440:Hemofiltration; D018836:Inflammation Mediators / Q000097:blood*; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D019332:Endothelin-1; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D015121:6-Ketoprostaglandin F1 alpha