Hemodynamic changes caused by glibenclamide in isolated, working, erythrocyte perfused rat heart

Glibenclamide-induced cardiac hemodynamic changes before and after ischemia have been frequently studied. In general a Langendorff buffer perfused heart model was used to examine these effects. However these models used protein-free buffer perfusates. To improve clinical relevance and thereby enhance extrapolation to the in vivo condition we studied the effects of glibenclamide on cardiac hemodynamics using a working, erythrocyte perfused, rat heart model, where the perfusate was enriched with albumin. The results show a dose-dependent decline in CBF in normoxia and at the end of reperfusion (after an ischemic period) with glibenclamide treatment compared to control. Cardiac functional recovery improved with 1 and 4 mumol.L-1 glibenclamide concentrations. From this study it seems that there is a marked decrease in CBF but this did not result in impaired myocardial function after a period of ischemia, so it appears that there are no startling side effects of glibenclamide in the ischemic rat heart.