Albumin influences total plasma antioxidant capacity favorably in patients with acute lung injury.
OBJECTIVE
To ascertain the influence of albumin on antioxidant status in patients with acute lung injury.


METHODS
Prospective, randomized, placebo-controlled study.


METHODS
Intensive care units, teaching hospitals.


METHODS
Twenty patients meeting the American European Consensus criteria for acute lung injury.


METHODS
Ten patients received albumin (25 g of a 25% solution every 8 hrs for a total of nine doses) and ten received placebo (normal saline administered in identical fashion and volume). All received supportive therapy appropriate for patients with acute lung injury. Plasma samples were obtained sequentially from all patients before, 30 mins after, and 4 hrs after albumin/placebo administration.


RESULTS
Serum albumin and total protein, total antioxidant status, iron-binding antioxidant protection, iron-oxidizing antioxidant protection, lipid hydroperoxides, protein carbonyls, and plasma thiols were measured. Albumin administration increased plasma albumin concentrations (p <.05 compared with placebo) and decreased concentrations of protein carbonyls (p <.05 compared with placebo). By contrast, plasma lipid hydroperoxide concentrations were similar in both groups, both in absolute terms and relative to albumin content. For all other variables, no significant differences were apparent. For all patients, there was a positive correlation between albumin and plasma thiol concentrations (r =.983, p <.01) and albumin and antioxidant capacity (r =.885, p =.01). In the albumin treatment group, there was a strong correlation between thiols and antioxidant capacity (r =.876, p =.01). No such correlation was apparent in the placebo group. Plasma iron-binding antioxidant protection was negatively correlated (r = -.741, p <.05) with albumin content in the treatment group but not the placebo group.


CONCLUSIONS
In patients with acute lung injury, albumin administration favorably influences plasma thiol-dependent antioxidant status as well as levels of protein oxidative damage.
Quinlan
Gregory J
GJ
Unit of Critical Care, Imperial College School of Medicine, Royal Brompton Hospital, London, UK.
Mumby
Sharon
S
Martin
Greg S
GS
Bernard
Gordon R
GR
Gutteridge
John M C
JM
Evans
Timothy W
TW
D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000975:Antioxidants / Q000378:metabolism*; D005260:Female; D006801:Humans; D007501:Iron / Q000097:blood; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000401:mortality / Q000628:therapy*; D012709:Serum Albumin / Q000627:therapeutic use*; D018709:Statistics, Nonparametric; D013438:Sulfhydryl Compounds / Q000037:antagonists & inhibitors / Q000097:blood; D014481:United States / Q000453:epidemiology
D000975:Antioxidants; D012709:Serum Albumin; D013438:Sulfhydryl Compounds; D007501:Iron