Albumin limits mesenteric endothelial dysfunction and inflammatory response in cardiopulmonary bypass.
The aim of this study was to investigate the potential anti-inflammatory and endothelial protective properties of albumin during cardiopulmonary bypass (CPB) in an experimental porcine model. Two groups underwent CPB for 90 min (n = 7 in each group), and a baseline (BL) control group did not undergo CPB (n = 7). Priming consisted of a gelatin solution (4% gelofusine, CPBG group) or colloid solution (5% albumin, CPBA group). Mesenteric arterial segments were isolated and exposed in vitro to phenylephrine (with or without nitric oxide synthase inhibition) to assess contractility, and exposed to acetylcholine and sodium nitroprusside to assess relaxation. Plasma tumor necrosis factor (TNF)-α levels, intestinal and pulmonary TNF-α and heme oxygenase (HO)-1 mRNA expression, and organ injury were studied. Upon sacrifice, TNF-α levels were significantly higher in the CPBG group than in the CPBA and BL groups. The contractile response was significantly higher in the CPBG group, whereas the response to acetylcholine was significantly lower in the CPBG group than in the other groups. HO-1 mRNA expression was significantly higher in intestine samples in the CPBA group than in the CPBG and BL groups. HO-1 mRNA expression was significantly higher in lung samples in the CPBA group than in the CPBG group. Leukocyte infiltration was significantly higher in intestine and lung samples in the CPBG group than in the CPBA and BL groups. Albumin priming reduced CPB-induced mesenteric vascular dysfunction and prevented the development of a systemic inflammatory response by modeling HO-1 expression in target organs.
INSERM U, Rouen Biomedical Research Institute, France. fabien.doguet@chu-rouen.fr
Fabien
F
Doguet
Fabienne
F
Tamion
Vincent
V
Le Guillou
Michael
M
Bubenheim
Christian
C
Thuillez
Vincent
V
Richard
Jean Paul
JP
Bessou
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002315:Cardiopulmonary Bypass / Q000379:methods*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D015870:Gene Expression / Q000187:drug effects; D051547:Heme Oxygenase-1 / Q000235:genetics; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008638:Mesenteric Arteries / Q000187:drug effects* / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics; D012709:Serum Albumin / Q000627:therapeutic use*; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology*; D014661:Vasoconstriction / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D012333:RNA, Messenger; D012709:Serum Albumin; D014409:Tumor Necrosis Factor-alpha; D051547:Heme Oxygenase-1