Profound haemodilution during normothermic cardiopulmonary bypass influences neither gastrointestinal permeability nor cytokine release in coronary artery bypass graft surgery

Abstract

Background: Cardiopulmonary bypass (CPB) impairs intestinal barrier function and induces systemic inflammation after cardiac surgery. The objective of this study was to evaluate the effect of profound haemodilution (haematocrit 19-21%) during normothermic CPB on gastrointestinal permeability and cytokine release in comparison with a standard haemodilution (haematocrit 24-26%).

Methods: This was a prospective, controlled, randomized pilot trial of 60 patients without gastrointestinal disease undergoing normothermic CPB (35.5-36 degrees C) for coronary artery bypass graft surgery. Gastrointestinal permeability was measured by the triple-sugar technique (sucrose, lactulose, and mannitol excretion in urine) before and after CPB. Interleukin (IL)-6, IL-10, and tumour necrosis factor alpha (TNFalpha) were quantified using enzyme-linked immunosorbent assays.

Results: Data from 59 patients (19-21% haematocrit, n=28; 24-26% haematocrit, n=31) were analysed. Data on gastrointestinal permeability were available for 47 patients (19-21% haematocrit, n=23; 24-26% haematocrit, n=24), blood samples for cytokine analysis from 59 patients. Mannitol excretion was normal before and after surgery without significant differences between the groups (after operation: 5.4% vs 2.9%, P=0.193). Lactulose and sucrose excretion was within a normal range before surgery and increased afterwards without differences between the groups. IL-6, IL-10, and TNFalpha were elevated after surgery, but there was no difference between the groups [IL-6 (P=0.78), IL-10 (P=0.74), and TNFalpha (P=0.67)].

Conclusions: Profound haemodilution during normothermic CPB brought about significant changes neither in intestinal permeability nor in cytokine release. It may be concluded that a haematocrit of 19-21% during normothermic CPB does not impair intestinal barrier function and cytokine response in patients without gastrointestinal comorbidity.