Irreversible hemorrhagic shock: treatment and cardiac pathophysiology.

Anesthetized dogs were subjected to hypotension at 35 mm Hg mean arterial pressure for 3 hours according to Wiggers' modified technique. One group of dogs received IV fructose-1,6-diphosphate (FDP) while the other group received equimolar glucose throughout the oligemic period. At 3 hours of hypotension, five glucose-treated and six dogs that received FDP were sacrificed for determination of myocardial ATP, creatine phosphate, and lactic acid tissue content. The remaining 14 dogs (six glucose-treated and eight FDP-treated) were retransfused with the shed blood and allowed to recover. The mean arterial pressure measured at 1 1/2 hours posttransfusion in the FDP-treated group returned to control values while the glucose controls remained 34 mm Hg below control. All controls had EKG ischemic changes, whereas no such changes were observed in the FDP-treated group. Endocardial ATP and creatine phosphate content in the controls were depleted to the same degree as found in acute myocardial ischemia, whereas in the FDP-treated dogs they were nearly normal range. All six retransfused dogs treated with glucose died, whereas all eight dogs that received FDP survived and had normal bowel and renal function and no apparent neurological deficit. These data indicate that FDP appears to be a potential therapeutic agent in the treatment of irreversible hemorrhagic shock by intervening in the Embden-Meyerhof pathway both as a metabolic regulator and high energy substrate.