Potential Relationships of Changes in Cell Transport and Metabolism in Shock

Abstract

Circulatory failure or shock is known to produce metabolic changes, including anaerobiosis with increased lactate production, a reduction in ATP stores, and an increase in inorganic phosphate. These changes indicate only a lack of availability of oxygen with depression of the Kreb’s cycle and electron transport system which should be reversible if blood flow or oxygen supply is restored. Ultimately, however, there must be not only a depression of cell function with shock but alterations and aberrations which may limit or destroy the cell’s capabilities even if its environment is improved. Early studies of mitochondrial metabolism in shock were reviewed by Levinson et al. in 1961,⁸ and they concluded that no significant changes in these cell systems had been found. Hift and Strawitz⁶ found normal P/O ratios in liver mitochondria of dogs subjected to severe hemorrhagic shock, although oxygen uptake was found to be higher than normal. DePalma et al.⁴ also demonstrated a lack of alteration of the P/O ratio of liver mitochondria with severe hemorrhagic shock using succinate as a substrate.