Continuous venovenous hemofiltration improves arterial oxygenation in endotoxin-induced lung injury in pigs.
BACKGROUND
Hypoxemia is common in septic acute lung failure. Therapy is mainly supportive, and most trials using specific inhibitors of key inflammatory mediators (ie., tumor necrosis factor alpha, interleukin 1) have failed to prove beneficial. The authors investigated if a nonspecific blood purification technique, using zero-balanced high-volume continuous venovenous hemofiltration (CWH), might improve arterial oxygenation in a fluid-resuscitated porcine model of endotoxin-induced acute lung injury.


METHODS
Piglets of both sexes weighing 25-30 kg were anesthetized and mechanically ventilated. After baseline measurements, animals received an intravenous infusion of 0.5 mg/kg endotoxin (Escherichia coli lipopolysaccharide). One hour after endotoxin, animals were randomly assigned to either treatment with CWH (endotoxin + hemofiltration, n = 6) or spontaneous course (endotoxin, n = 6). At 4 h after randomization, animals were killed. Hemofiltration was performed from femoral vein to femoral vein using a standard circuit with an EF60 polysulphone hemofilter.


RESULTS
Endotoxin challenge induced arterial hypoxemia, an increase in peak inspiratory pressure, pulmonary hypertension, and systemic hypotension. Treatment with CWH did not improve systemic or pulmonary hemodynamics. However, arterial oxygenation was increased in endotoxin-challenged animals at 5 h after completion of endotoxin infusion, as compared with animals not receiving CVVH (arterialoxygen tension, 268+/-33 vs. 176+/-67 mm/Hg, respectively, P < 0.01). In addition, treatment with CWH attenuated the endotoxin-induced increase in peak inspiratory pressure and increased lung compliance.


CONCLUSIONS
These results suggest that nonspecific blood purification with high-volume CWH improves arterial oxygenation and lung function in endotoxin-induced acute lung injury in pigs, independent of improved hemodynamics, fluid removal, or body temperature.
Ullrich
R
R
Department of Anesthesiology and General Critical Care Medicine, Vienna General Hospital, University of Vienna, Austria. roman.ullrich@univie.ac.at
Roeder
G
G
Lorber
C
C
Quezado
Z M
ZM
Kneifel
W
W
Gasser
H
H
Schlag
G
G
Redl
H
H
Germann
P
P
D000818:Animals; D001784:Blood Gas Analysis; D003404:Creatinine / Q000097:blood; D004731:Endotoxins; D005260:Female; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006440:Hemofiltration; D019344:Lactic Acid / Q000097:blood; D008168:Lung / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D010100:Oxygen / Q000097:blood*; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D015656:Respiratory Mechanics / Q000187:drug effects; D013552:Swine; D014882:Water-Electrolyte Balance / Q000502:physiology
D004731:Endotoxins; D009566:Nitrates; D009573:Nitrites; D017472:Receptors, Interleukin-1; D019344:Lactic Acid; D003404:Creatinine; D010100:Oxygen