| First Author | MacGowan GA | Year | 2001 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 281 |
| Issue | 6 | Pages | H2539-48 |
| PubMed ID | 11709421 | Mgi Jnum | J:134703 |
| Mgi Id | MGI:3789547 | Doi | 10.1152/ajpheart.2001.281.6.H2539 |
| Citation | MacGowan GA, et al. (2001) Compensatory changes in Ca(2+) and myocardial O(2) consumption in beta-tropomyosin transgenic hearts. Am J Physiol Heart Circ Physiol 281(6):H2539-48 |
| abstractText | Transgenic mice overexpressing beta-tropomyosin have increased myofilament Ca(2+) sensitivity that we hypothesized would result in altered relationships among pressure and heart rates, intracellular Ca(2+), and myocardial O(2) consumption. In perfused hearts from transgenic mice there was a marked negative force-frequency response between 6 and 10 Hz with a 30 +/- 3% reduction in peak-positive first derivative of pressure development over time (dP/dt) compared with 14 +/- 2% in wild-type mice (P < 0.001). At 8 Hz systolic pressures were normal, though peak systolic intracellular Ca(2+) was significantly reduced in transgenic mice versus wild type (726 +/- 61 vs. 936 +/- 67 nM, P < 0.05) indicating an alteration in the pressure-Ca(2+) relationship. Over a wide range of positive and negative inotropic interventions there were normal developed pressures, though marked elevations in myocardial O(2) consumption (15-54%). Because pressures are normal and intracellular Ca(2+) decreased and myocardial O(2) consumption increased, this suggests that these abnormalities are at least in part compensatory mechanisms to the altered myofilament function. |
