Effects of fructose-1,6-diphosphate, glucose, and saline on cardiac resuscitation

Abstract

Severe hypoxemia causes respiratory and cardiac arrest, in part, because severe hypoxemia decreases glycolysis and adenosine triphosphate (ATP) production by a lactic acid-induced decrease in the activity of phosphofructokinase and glyceraldehyde-3-P dehydrogenase. Fructose-1,6-diphosphate (FDP) administration increases the ATP concentration of blood. The authors hypothesized that FDP might increase the number of rabbits that could be resuscitated from hypoxemic cardiac arrest. To test this hypothesis, heart rate, arterial pressure, left ventricular end-diastolic pressure, and blood gases and pH were measured during normoxemia (FI(O2) = 0.21) and again during hypoxemia (FI(O2) = 0.04) in 28 adult, white, New Zealand rabbits anesthetized with pentobarbital. With the onset of hypoxemia, we gave either 40 mg/kg of 5% FDP (n = 10), 5% glucose (n = 11), or an equal volume (2.5 ml) of normal saline (n = 7) intravenously and began a continuous infusion of 2.0 mg·kg-1·min-1 of the same sugar or 0.12 ml/min of saline. FDP-treated rabbits breathed for 20.9 ± 4.9 (mean ± SEM) min after initiation of hypoxemia; glucose-treated rabbits breathed for 1.4 ± 0.2 min, and saline-treated rabbits breathed 10.3 ± 4 min. Cardiac arrest occurred 2.5 ± 0.5 min after the onset of respiratory arrest in FDP-treated rabbits, 4.1 ± 0.2 min in glucose-treated rabbits, and 2.9 ± 0.4 min in saline-treated rabbits. We could resuscitate all ten FDP-treated rabbits; two of 11 glucose-treated (FDP vs. glucose, P < 0.001); and one of seven saline-treated rabbits (FDP vs. saline, P < 0.001) from cardiac arrest. It is concluded that FDP prolongs the time to respiratory arrest and increases immediate salvage from cardiac arrest in severely hypoxemic, adult rabbits.