Journal of Applied Physiology AJP: Cell Physiology
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J Appl Physiol 81: 1834-1842, 1996;
8750-7587/96 $5.00
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Journal of Applied Physiology
Vol. 81, No. 4, pp. 1834-1842, October 1996
SYSTEMIC CIRCULATION AND FLUID BALANCE

Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by PCO2

Ranna A. Rozenfeld, Michael K. Dishart, Tor Inge Tønnessen, and Robert Schlichtig

Departments of Anesthesiology and Critical Care Medicine, Internal Medicine, and Surgery, University of Pittsburgh, and Veterans Affairs Medical Center, Pittsburgh, Pennsylvania 15240

Received 4 November 1994; accepted in final form 13 May 1996.

Rozenfeld, Ranna A., Michael K. Dishart, Tor Inge Tønnessen, and Robert Schlichtig. Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by PCO2. J. Appl. Physiol. 81(4): 1834-1842, 1996.---Gut ischemia is often assessed by computing an imaginary tissue interstitial pH from arterial plasma HCO-3 and the PCO2 in a saline-filled balloon tonometer after equilibration with tissue PCO2 (PtiCO2). PtiCO2 may alternatively be assumed equal to venous PCO2 (PvCO2) in that region of gut. The idea is that as blood flow decreases, gut PtiCO2 and PvCO2 will increase to the maximum aerobic value, i.e., maximum respiratory PvCO2 (PvCO2 rmax). Above a "critical" anaerobic threshold, lactate (La-) generation, by titration of tissue HCO-3, should raise PtiCO2 above PvCO2 rmax. During progressive selective whole intestinal flow reduction in six pentobarbital-anesthetized pigs, we used PCO2 electrodes to test the hypotheses that critical PtiCO2 is achieved earlier in mucosa than in serosa and that PvCO2 rmax, computed using an in vitro model, predicts critical PtiCO2. We defined critical PtiCO2 as the inflection of PtiCO2-PvCO2 vs. O2 delivery (QO2) plots. Critical QO2 for O2 uptake was 12.55 ± 2 ml · kg-1 · min-1. Critical PtiCO2 for mucosa and serosa was achieved at similar whole intestine QO2 (13.90 ± 5 and 13.36 ± 5 ml · kg-1 · min-1, P = NS). Critical PtiCO2 (129 ± 24 and 96 ± 21 Torr) exceeded PvCO2 rmax (62 ± 3 Torr). During ischemia, La- excretion into portal venous blood was matched by K+ excretion, causing PvCO2 to increase only slightly, despite PtiCO2 rising to 380 ± 46 (mucosa) and 280 ± 38 (serosa) Torr. These results suggest that mucosa and serosa become dysoxic simultaneously, that ischemic dysoxic gut is essentially unperfused, and that in vitro predicted PvCO2 rmax underestimates critical PtiCO2.

ischemia; acidosis; carbon dioxide; hypercarbia; strong ion difference


0161-7567/96 $5.00 Copyright © 1996 the American Physiological Society




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