Abstract
It has been hypothesized (Nelson et al., 1988, Samsel et al., 1988, Bredle et al. 1989), that sepsis is a disorder of microvascular regulation resulting in decreased O2 transport from the capillaries to the mitochondria. Evidence for this hypothesis was offered by Nelson et al. (1988), who found greater levels of systemic and intestinal critical O2 transport (TO2), defined as the minimum TO2 required to maintain constant O2 consumption (VO2), in hypovolemic septic dogs when compared to a control group. This phenomenon may be related to increases in microcirculatory heterogeneity, resulting in a mismatch of tissue perfusion and cellular O2 needs. This is manifested at the organ level by decreases in O2 extraction capacity.
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© 1990 Plenum Press, New York
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Gutierrez, G., Lund, N., Palizas, F., Acero, A. (1990). Skeletal Muscle PO2 during Hypodynamic Sepsis. In: Piiper, J., Goldstick, T.K., Meyer, M. (eds) Oxygen Transport to Tissue XII. Advances in Experimental Medicine and Biology, vol 277. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8181-5_63
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DOI: https://doi.org/10.1007/978-1-4684-8181-5_63
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