Background. Glucose, insulin, and potassium solution improves left ventricu
lar function in refractory pump failure. Direct effects of insulin on the h
eart cannot be determined in vivo. We hypothesized that insulin has a direc
t positive inotropic effect on the reperfused heart.
Methods. Isolated working rat hearts were perfused with buffer containing g
lucose (5 mmol/L) plus oleate (1.2 mmol/L). Hearts were subjected to 15 min
utes of ischemia and reperfused with or without insulin (100 mu U/mL) for 4
0 minutes. Epinephrine (1 mu mol/L) was added for the last 20 minutes.
Results. Hearts recovered 51.1% of preischemic cardiac power in the absence
and 76.4% in the presence of insulin (p < 0.05). Whereas oleate oxidation
remained unchanged, glucose uptake and oxidation increased during reperfusi
on with epinephrine (p < 0.01). This increase was significantly greater whe
n hearts were reperfused in the presence of insulin (p < 0.01). Insulin als
o prevented an epinephrine-induced glycogen breakdown during reperfusion (p
< 0.05).
Conclusions. Insulin has a direct positive inotropic effect on postischemic
rat heart. This effect is additive to epinephrine and occurs without delay
. Increased rates of glucose oxidation and net glycogen synthesis are more
protracted. (C) 1999 by The Society of Thoracic Surgeons.