Fig. 5.
Impaired function of isolated Hif-1α+/- cardiomyocytes after transverse aortic constriction (TAC). Cardiomyocytes were isolated from male Hif-1α+/+ and Hif-1α+/− mice 3 weeks after TAC or sham-intervention. Cells were stimulated with 1–4 Hz and were analyzed for a fractional shortening, which was measured as percent resting cell length (RCL) after TAC treatment (*p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/+ versus TAC-treated Hif-1α+/− mice), b Ca2+ transient amplitude (*p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/− versus sham-treated Hif-1α+/− mice), c RT 50% [Ca2+]i decline (*p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/− versus sham-treated Hif-1α+/− mice, # p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/+ versus sham-treated Hif-1α+/+ mice), d RT 50% twitch relaxation (*p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/− versus sham-treated Hif-1α+/− mice, # p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/+ versus sham-treated Hif-1α+/+ mice) and e SR Ca2+ content measured by caffeine-induced Ca2+ transients (*p < 0.05 cardiomyocytes derived from TAC-treated Hif-1α+/− versus sham-treated Hif-1α+/− mice). f Protein extracts derived from hearts of Hif-1α+/+ and Hif-1α+/− mice were analyzed by immunoblots