BACKGROUND: JTV519 is know to protect cardiomyocytes from calcium 
overloading-induced damage. The aim of this study was to investigate the 
potential protective effect of JTV519 on myocardium subjected to prolonged 
ischemia and the underlying mechanism of such protection. The effect of JTV519 
was also compared with that of diltiazem, a 1,5-benzothiazepine derivative.
METHODS: Isolated rat hearts were randomly divided into three groups. Control 
hearts were arrested with histidine-tryptophan-ketoglutarat (HTK) cardioplegic 
solution alone. In the JTV519 group of hearts, cardiac arrest was achieved with 
JTV519 (10(-3) mmol/L) in the HTK solution. Hearts in the diltiazem group were 
arrested with diltiazem (0.5 mmol/L) in the HTK solution. All the hearts were 
then subjected to 6-hour storage in HTK solution at 4 degrees C.
RESULTS: After a 30-minute reperfusion, the left ventricular developed pressure 
in the JTV519 and diltiazem groups were improved significantly compared with the 
control group. There was a significantly lower left ventricular end-diastolic 
pressure level and higher recovery of coronary flow in the JTV519 group than in 
the control group. The postischemic intracellular calcium concentration was 
attenuated by adding JTV519 or diltiazem to HTK cardioplegia.
CONCLUSION: As an adjunct to cardioplegia, JTV519 showed a significant 
protective effect on myocardium undergoing 6 hours of ischemia. The beneficial 
protective effects of JTV519 are correlated with its ability to inhibit the 
postischemic rise in intracellular calcium.