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J Appl Physiol 87: 933-937, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 3, 933-937, September 1999

Effects of hyper- and hypoventilation on gastric and sublingual PCO2

Andrej Pernat1, Max Harry Weil1,2, Wanchun Tang1,2, Hitoshi Yamaguchi1, Andreja Marn Pernat1, Shijie Sun1,2, and Joe Bisera1,2

1 Institute of Critical Care Medicine, Palm Springs 92262; and 2 University of Southern California School of Medicine, Los Angeles, California 90033

We investigated the effects of hyper- and hypoventilation on gastric (PgCO2) and sublingual (PslCO2) tissue PCO2 before, during, and after reversal of hemorrhagic shock. PgCO2 was measured with ion-sensitive field-effect transistor sensor and PslCO2 with a CO2 microelectrode. Under physiological conditions and during hemorrhagic shock, decreases in arterial (PaCO2) and end-tidal (PETCO2) PCO2 induced by hyperventilation produced corresponding decreases in PgCO2 and PslCO2. Hypoventilation produced corresponding increases in PaCO2, PETCO2, PgCO2, and PslCO2. Accordingly, acute decreases and increases in PaCO2 and PETCO2 produced statistically similar decreases and increases in PgCO2 and PslCO2. No significant changes in the tissue PCO2-PaCO2 gradients were observed during hemorrhagic shock in the absence or in the presence of hyper- or hypoventilation. Acute changes in PgCO2 and PslCO2 should, therefore, be interpreted in relationship with concurrent changes in PaCO2 and/or PETCO2.

tissue carbon dioxide tension; hyperventilation; hemorrhagic shock


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