Postischemic cardiac failure may be associated with inadequate storage of myocardlal adenosine triphosphate (ATP). ATP precursors were administered to resuscitate the postischemic myocardium.
Hearts Isolated from male Wistar adult rats were perfused with Krebs-Henseleit buffer (pH, 7.40), subjected to 30 minutes of global ischemia at 36°C, followed by 30 minutes of retrograde reperfusion with the postischemic intervention of ruthenium red (1 μM), ribose (1 mM), and adenine (1 mM). Multiple analysis of variance was used to compare means between groups (eight rats in each group).
In comparison with the nonischemic group, the postischemic nontreated group had a decrease in the maximum rate of left ventricular pressure rise (+dP/dt, P<0.0005) and level of myocardial ATP (P<0.0005) but an increase in level of mitochondrial Ca2+ (P<0.005). In comparison with the nontreated group, ribose and adenine had no effect on all the above-mentioned parameters, and ruthenium red elevated maximum left ventricular +dP/dt (P<0.05) and reduced mitochondrial Ca2+ (P<0.05) with no change in ATP (P>0.05). However, ruthenium red with ribose and adenine achieved a significant increase in maximum left ventricular +dP/dt (P<0.0005), ATP levels (P<0.005), and a decrease in levels of mitochondrial Ca2+ (P<0.005).
Acute postischemic cardiac failure may be related to Ca2+ overload in mitochondria. Ruthenium red may reduce mitochondrial Ca2+ overload. Ruthenium red, ribose, and adenine in combination may be capable of enhancing the recovery of myocardial high-energy phosphates and mechanical function in the postischemic myocardium.