Failure of nicotinamide in the treatment of hemorrhagic shock

IH Chaudry, S Zweig, MM Sayeed, AE Baue - Journal of Surgical Research, 1976 - Elsevier
IH Chaudry, S Zweig, MM Sayeed, AE Baue
Journal of Surgical Research, 1976Elsevier
Hemorrhagic shock in rats was produced by bleeding the animals to a mean arterial
pressure of 40 mm Hg which was maintained for 1.5 hr. ATP, ADP, and NAD (nicotinamide
adenine dinucleotide) levels decreased and NADH (reduced pyridine nucleotide) levels
increased significantly in liver and kidney of such animals. Infusion of NAD, nicotinamide, or
nicotinic acid following shock increased the tissue NAD and decreased the NADH levels.
Under ideal conditions, the oxidation of NADH to NAD should result in phosphorylation of …
Abstract
Hemorrhagic shock in rats was produced by bleeding the animals to a mean arterial pressure of 40 mm Hg which was maintained for 1.5 hr. ATP, ADP, and NAD (nicotinamide adenine dinucleotide) levels decreased and NADH (reduced pyridine nucleotide) levels increased significantly in liver and kidney of such animals. Infusion of NAD, nicotinamide, or nicotinic acid following shock increased the tissue NAD and decreased the NADH levels. Under ideal conditions, the oxidation of NADH to NAD should result in phosphorylation of ADP. Thus more ATP would be expected to be present. However, infusion of the above compounds failed to affect the tissue ATP levels after shock. Failure of animals to survive shock despite increases in tissue NAD levels following NAD, nicotinamide, or nicotinic acid infusion suggests that these infusions have no salutary effect in hemorrhagic shock.
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