Attenuation of ischemia-reperfusion induced changes in cardiac performance and sarcoplasmic reticulum function by vanadate.

By virtue of its ability to enhance glucose uptake and oxidation in the cell, vanadate is known to exert an insulin-like action in the body. Because defects in substrate use and energy generation are considered to play an important role in cardiac contractile dysfunction as a consequence of ischemia-reperfusion (I/R), this study was carried out to examine the effects of vanadate on I/R-induced changes in cardiac performance and sarcoplasmic reticulum (SR) function. For this purpose, isolated rat hearts were subjected to global ischemia for 30 min and then reperfused for 30 min with normal perfusion medium in the absence or presence of different concentrations of vanadate. The left ventricular developed pressure, rate of contraction and rate of relaxation were depressed, whereas the left ventricular end-diastolic pressure was increased in the ischemic-reperfused heart. However, these abnormalities were attenuated on treatment of the heart with 1 muM and 4 muM of vanadate. The SR preparation isolated from the ischemic-reperfused hearts showed a marked depression in calcium uptake and ryanodine binding (calcium release channel) activities; these defects were attenuated by the addition of vanadate to the perfusion medium. The results demonstrate beneficial effects of vanadate on cardiac dysfunction and changes in SR calcium transport due to I/R injury.