Objective: We hypothesized that reduction of 棺1 integrins in the cardiac myocyte would predispose the adult mouse heart to decreased functional recovery of the left ventricle (LV) following ischemia/reperfusion (I/R) injury. For this we used cardiac-specific conditional knock-out(CKO) of 棺1 integrin. Methods and Results: 棺1 integrin cardiac-specific CKO, (慣MHC/MerCreMer,棺1flox/flox) as C57BL/6 were studied at 8- to 12-weeks of age. Tamoxifen(Tamo) was injected intraperitoneally(n=9) once per day for five consecutive days. Mice of the same genotype injected with corn oil were used as controls(n=8). Additional controls were 棺1flox/flox, mice administered Tamo(n=3). 30 days following the last Tamo injection, Western blot showed 76% reduction of 棺1 integrin protein in CKO 棺1 integrin hearts, compared with control groups. Only mild fibrosis of myocardium was noted in CKO 棺1 integrin hearts. The isolated heart were subjected to 20 minutes of no-flow global ischemia, followed by 40 minutes of reperfusion. The creatine kinase level in the effluent collected from CKO 棺1 integrin hearts increased more than controls (n=4, each group), though statistic significane was not noted.. Baseline LV developed pressure(LVDP) and heart rate(HR) were not significantly different among groups. Post-reperfusion recovery of LVDP at 40 min was significantly worse in CKO 棺1 integrin hearts(22짹2%) than control hearts(57짹2% and 57짹3%, p<0.05). Post-reperfusion recovery of rate pressure product(RPP=LVDP x HR) was also significantly worse in CKO 棺1 integrin hearts(22짹2%) than in control group hearts(53짹2% and 50짹3%, p<0.05). Conclusions: Our results show that 棺1 integrin plays an important role in functional recovery after acute I/R injury. Future studies are aimed at elucidating the mechanism that short-term reduction (1 month) of myocyte 棺1 integrin causes impaired recovery of LV function after I/R injury.