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February 1974

Depletion and Restoration of Tissue ATP in Hemorrhagic Shock

Author Affiliations

St. Louis
From the Division of Cell Physiology and the Department of Surgery, Washington University School of Medicine; and The Jewish Hospital of St. Louis (Drs. Chaudry, Sayeed, and Baue).

Arch Surg. 1974;108(2):208-211. doi:10.1001/archsurg.1974.01350260062014

Hemorrhagic shock was produced in conscious rats by bleeding the animals to a mean arterial pressure of 40 mm Hg that was maintained for 1½ hours. At the end of the shock period, the animals received (1) blood alone; or (2) blood plus Ringer lactate; or (3) adenosine triphosphate-magnesium chloride (ATP-MgCl2) followed by blood; or (4) adenosine diphosphate-MgCl2 (ADP-MgCl2), or adenosine phosphate-MgCl2 (AP-MgCl2), or adenosine-MgCl2 followed by blood and were killed three minutes afterward. Analysis of liver and kidney showed that ATP levels decreased during shock, and they remained low when blood, blood plus Ringer lactate or ADP-MgCl2, AP-MgCl2, or adenosine-MgCl2 were given. Adenosine triphosphate levels returned to normal in both tissues only when ATP-MgCl2 and blood were given. The effect of ATP-MgCl2 in restoring ATP levels of liver and kidney may be through provision of the high-energy phosphate compound.