Intramucosal-arterial PCO2 gap fails to reflect intestinal dysoxia in XXXX .

@entity11126 @entity742 @entity548 @entity5836 @entity26 @entity7853 @entity519 @entity9595
INTRODUCTION: An elevation in intramucosal-arterial PCO2 gradient (DeltaPCO2) could be determined either by tissue @entity519 or by reduced blood flow. Our hypothesis was that in @entity519 with preserved blood flow, DeltaPCO2 should not be altered. METHODS: In 17 anesthetized and mechanically ventilated @entity742 , @entity26 delivery was reduced by decreasing flow ( @entity7853 , @entity11126 ) or arterial @entity26 saturation ( @entity519 , @entity9595 ), or no intervention was made (sham). In the @entity11126 group (n = 6), blood flow was lowered by stepwise @entity548 ; in the @entity9595 group (n = 6), @entity5836 was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and @entity26 saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO2 by tonometry. Systemic and intestinal @entity26 transport and consumption were calculated, as was DeltaPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. RESULTS: Both progressive @entity548 and @entity5836 aspiration provoked critical reductions in systemic and intestinal @entity26 delivery and consumption. No changes occurred in the sham group. DeltaPCO2 increased in the @entity11126 group (12 +/- 10 [mean +/- SD] versus 40 +/- 13 mmHg; P < 0.001), but remained unchanged in @entity9595 and in the sham group (13 +/- 6 versus 10 +/- 13 mmHg and 8 +/- 5 versus 9 +/- 6 mmHg; not significant). DISCUSSION: In this experimental model of @entity519 with preserved blood flow, DeltaPCO2 was not modified during dependence of @entity26 uptake on @entity26 transport. These results suggest that DeltaPCO2 might be determined primarily by blood flow.
