FIG. 3.

LV function ex vivo. To ensure that differences in LV function measured in vivo were not influenced by the effects of anesthesia, vasodilation, or autonomic reflexes, isolated perfused hearts were studied. Six weeks after AAV8.UCn2 (5×10¹¹ GC, intravenous) or saline (CON) administration, hearts were isolated and perfused and LV pressure was measured, blinded to group identity. (A) AAV8.UCn2 increased LV developed pressure. (B and C) LV +dP/dt (B), and LV −dP/dt (C) were increased in hearts from mice that had received AAV8.UCn2, confirming data obtained in vivo (Fig. 2 and Table 2). (D) Heart rates were not different between groups. These data (A–D) confirm that alterations in systolic and diastolic function are intrinsic to the heart, and do not reflect vasodilation due to increased levels of urocortin-2 alone. In all graphs, data represent means±SE, and numbers in columns denote group size. Values of p were determined by Student t test (unpaired, two-tailed).