Nicotinamide adenine dinucleotides were determined in the liver of rats subjected to three stages of hemorrhagic shock and treatment. Total nucleotide content was decreased in all stages. The oxidized form, NAD⁺, appeared to decrease more rapidly than the reduced form, NADH; however this was likely the result of a shift from oxidized to reduced state due to decreased tissue perfusion. Increased enzymic degradation of NAD did not appear to be the mechanism whereby NAD content was lowered; NADase activity of shock liver was not different from that of control liver. These results also indicate that the decreased NAD content in shock is restored to normal by nonspecific treatment by replenishment of circulatory volume.

The authors are grateful for the technical assistance of Betty Henton and the clerical assistance of Gail Perry.