Fructose-1,6-bisphosphate improves efficiency of work in isolated perfused rat hearts

Abstract

The purpose of this study was to determine whether exogenous fructose-1,6-bisphosphate (F-1,6-P2) directly affects myocardial hemodynamics and certain metabolic parameters. Isolated working rat hearts were perfused for 30 min with 10 mM glucose (+insulin) as the exclusive exogenous substrate followed by 15 min with glucose plus one of the following concentrations (in mM) of F-1,6-P2: 1.25, 2.5, 5, or 10, and finally returned to the glucose only buffer. Additions of 2.5 and 5 mM F-1,6-P2 decreased (P less than 0.01) oxygen consumption (VO2) by 10.8 and 17.0% and coronary flow by 8.3 and 10.3%, respectively. No changes were observed in lactate release, cardiac output (CO), peak systolic pressure, heart rate, or pressure work (PW). Efficiency, expressed as PW divided by VO2, increased with F-1,6-P2 by 8.6% with 1.25 mM (P less than 0.05), 13.2% with 2.5 mM (P less than 0.01), and 16.9% with 5 mM (P less than 0.01). F-1,6-P2 at 10 mM produced no further improvements in VO2 or efficiency but was associated with declines (P less than 0.05) in CO and PW. Glucose plus 10 mM fructose had no effects on any of the above parameters, indicating that the F-1,6-P2-induced changes were not due to changes in osmolarity or to end products of F-1,6-P2 hydrolysis. Some chelation of buffer calcium by F-1,6-P2 occurred, but when free calcium was equalized in glucose and glucose plus 5 mM F-1,6-P2 buffers, the decline in VO2 (11.5%) was still far greater than could be explained by exogenous F-1,6-P2 metabolism in the glycolytic pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Fructose 1,6-Diphosphate Administration Attenuates Post-Ischemic Ventricular Dysfunction

“…It has been shown that administration of FDP improves the efficiency of the ex vivo rat heart and possibly protects against free radical damage. 5 Additionally, elevated creatine phosphate levels have been demonstrated in the isolated rat heart following FDP infusion, 6 illustrating biochemical evidence of FDP's benefit. In rabbits, it was shown that intravenous delivery of FDP prolonged the time to respiratory arrest and increased immediate salvage from cardiac arrest.…”

Effect of N-2-mercaptopropionyl glycine on exercise-induced cardiac adaptations

“…Myocardial function was evaluated 24 h after the last treatment using an isolated, working heart preparation. Rats were anesthetized with an intraperitoneal injection of 40 mg/kg pentobarbital sodium, and hearts were excised, weighed, and mounted on the perfusion apparatus, as previously described (37,38). The perfusate was a modified Krebs-Henseleit buffer containing (in mM): 10 glucose, 3.0 CaCl 2, 118.5 NaCl, 4.7 KCl, 1.2 MgSO4, 24.7 NaHCO3, 0.5 EDTA, and 12 IU/l insulin.…”

“…Myocardial oxygen consumption (V O2) was calculated from the arteriovenous difference in oxygen concentration multiplied by the coronary flow. Arterial oxygen concentration was maintained at 956 M, and venous oxygen concentration was continuously monitored by immediately diverting 5 ml/min of coronary effluent through an in-line Clark-type oxygen electrode, as previously described (37,38). Myocardial work efficiency was calculated by dividing external work by V O2 (37).…”

Analysis of Fructose 1,6-Diphosphate in Fermentation Broth Using Ion Chromatography

“…Subsequently, great efforts were made to study FDP physiological functions. It is known that FDP can enhance cell metabolism and cardiac myocyte nutrients, build up the resistance to convulsions, improve anoxic organ performance [3][4][5][6][7][8][9]. Now it is primarily used as a rescue drug for shock patients, in addition to, or used for angina pectoris, heart failure, myocardial infarction secondary treatment, in the cardiovascular acute and chronic disease treatment and prevention with an important role.…”