• S K Ohri, J Becket, J Brannan, B E Keogh, and K M Taylor.
• Department of Surgery, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom.
• Ann. Thorac. Surg. 1994 May 1; 57 (5): 1193-9.

AbstractStudies documenting rises in endotoxin after cardiopulmonary bypass (CPB) have postulated gut mucosal hypoperfusion. We have investigated alterations in jejunal blood flow by laser Doppler flow measurement, intramucosal pH (pHi) by tonometry, and oxygen utilization in a canine model of hypothermic CPB (n = 11 dogs). After 10 minutes of hypothermic CPB, despite no major reduction in superior mesenteric artery flow, mucosal laser Doppler flow decreased to -38.2% +/- 9.3% of levels obtained before bypass (p = 0.008) and serosal laser Doppler flow, to -47.3% +/- 11.4% (p = 0.006). During the hypothermic phase, mesenteric oxygen consumption fell from 0.18 +/- 0.01 to 0.098 +/- 0.01 mL.min-1.kg-1 (p = 0.005), and mesenteric oxygen delivery fell from 1.97 +/- 0.39 to 1.14 +/- 0.12 mL.min-1.kg-1 (p = 0.05). There was no change in jejunal pHi. During the rewarming phase, there was a substantial increase in mucosal laser Doppler flow, peaking at +69.8% +/- 15.2% (p = 0.03), whereas serosal laser Doppler flow returned to values seen prior to CPB (-16.4% +/- 21.5%; p = 0.25). These changes coincided with a surge in oxygen consumption (0.33 +/- 0.042 mL.min-1.kg-1; p = 0.009), while mesenteric oxygen delivery remained depressed at 1.09 +/- 0.12 mL.min-1.kg-1 (p = 0.04). Jejunal pHi fell from a value of 7.36 +/- 0.04 before CPB to 7.12 +/- 0.07 (p = 0.02), thus indicating mucosal hypoxia. During the rewarming phase of hypothermic CPB, there is a disparity between mesenteric oxygen consumption and oxygen delivery with villus tip ischemia; these findings may explain the pathophysiology of endotoxemia during CPB.

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