CARDIOPULMONARY BYPASS IMPAIRS SMALL-INTESTINAL TRANSPORT AND INCREASES GUT PERMEABILITY

Gastrointestinal damage occurs in 0.6% to 2% of patients after cardiop ulmonary bypass (CPB), and carries a mortality of 12% to 67%. The inci dence of subclinical gastrointestinal damage may be much greater. We e xamined the effects of nonpulsatile, hypothermic CPB on intestinal abs orption and permeability in 41 patients. Bowel mucosal saccharide tran sport and permeation were evaluated using 100 mL of an oral solution c ontaining 3-O-methyl-D-glucose (0.2 g), D-xylose (0.5 g), L-rhamnose ( 1.0 g), and lactulose (5.0 g) to assess active carrier-mediated, passi ve carrier-mediated, transcellular, and paracellular transport, respec tively, with a 5-hour urine analysis. Patients were studied before, im mediately after, and 5 days after CPB. Immediately after CPB there was a decrease in urinary excretion of 3-O-methyl-D-glucose (from 34% +/- 2.2% to 5.2% +/- 0.7%; p < 0.0001), D-xylose (from 25.4% +/- 1.4% to 4.1% +/- 0.8%; p < 0.0001), and L-rhamnose (from 8.3% +/- 0.6% to 2.6% +/- 0.4%; p < 0.0001). The permeation of 3-O-methyl-D-glucose and D-x ylose returned to normal levels 5 days after CPB, but that Of L-rhamno se remained significantly below pre-CPB values at 6.6% +/- 0.5% (p = 0 .004). However, the permeation of lactulose increased after CPB (from 0.35% +/- 0.04% to 0.59% +/- 0.1%; p = 0.018), and the lactulose/L-rha mnose gut permeability ratio increased markedly (from 0.045 +/- 0.04 t o 0.36 +/- 0.08; normal = 0.06 to 0.08; p = 0.004). Patients who had a CPB time of 100 minutes or more had a greater increase in gut permeab ility (p = 0.049). In 10 patients, gastric mucosal blood flow was dete rmined by laser Doppler flowmetry. A 48.7% +/- 7% reduction in gastric mucosal laser Doppler flow was found 30 minutes after the institution of CPB (p = 0.0001). This study demonstrates that after CPB gut barri er function is impaired, with increases in gut permeability; patients undergoing longer (>100 minutes) bypass procedures sustain greater inc reases in gut permeability. There is reversible impairment of small bo wel transcellular transport after CPB. The alterations in gut barrier function and mucosal transport are probably secondary to CPB-induced m ucosal hypoperfusion. These findings have implications for the prevent ion of endotoxemia after CPB, as well as enteral nutrition and drug th erapy in the immediate post-CPB period.