Abstract
Adams and Cain (1983) found that non-muscle regions of the body decreased their share of excess post-hypoxic oxygen uptake (\(\dot VO\)O2) with longer periods of hypoxia. They suggested that part of non-muscle \(\dot VO\)O2 was not obligated for energy production. Mortillaro and Granger (1977) showed that intestine followed a similar pattern of excess \(\dot VO\)O2 when arterial occlusion created an O2 deficit. Shepherd (1978) showed that an arterial PO2 of 46 Torr decreased intestinal \(\dot VO\)O2 26% but, in contrast, hindlimb \(\dot VO\)O2 was unaffected by an arterial PO2 of 36 Torr (Cain & Chapler, 1979) while, at the same time, whole body \(\dot VO\)O2 was decreased approximately 12%. These data, and the fact that gut \(\dot VO\)O2 is 20–25% that of whole body, even though intestine accounts for <5% of body weight, implicated gut as a bigger contributor of O2 excess used in recovery. Since Shepherd (1978) did not measure \(\dot VO\)O2 during recovery and Mortillaro and Granger (1977) did not use hypoxia, there was no information on the intestinal O2 deficit/excess relationship during and after hypoxia. In addition, its contribution to whole body O2 deficit/excess remained in question. Thus, the purposes of these experiments were to 1) measure the gut O2 deficit/excess relationship during acute hypoxic hypoxia, 2) determine the contribution of gut in whole body O2 deficit and excess and 3) ascertain the means by which intestine copes with acute bouts of hypoxic hypoxia.
This study was supported by grant #HL-26927, National Heart, Lung and Blood Institute.
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© 1986 Plenum Press, New York
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Dodd, S.L., King, C.E., Cain, S.M. (1986). Gut and Whole Body O2 Deficit during and Excess Uptake after Hypoxia. In: Longmuir, I.S. (eds) Oxygen Transport to Tissue VIII. Advances in Experimental Medicine and Biology, vol 200. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5188-7_55
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