| First Author | Min JY | Year | 2002 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 283 |
| Issue | 6 | Pages | H2466-71 |
| PubMed ID | 12388257 | Mgi Jnum | J:135478 |
| Mgi Id | MGI:3793915 | Doi | 10.1152/ajpheart.01062.2001 |
| Citation | Min JY, et al. (2002) Overexpression of Na+/Ca2+ exchanger gene attenuates postinfarction myocardial dysfunction. Am J Physiol Heart Circ Physiol 283(6):H2466-71 |
| abstractText | We monitored myocardial function in postinfarcted wild-type (WT) and transgenic (TG) mouse hearts with overexpression of the cardiac Na(+)/Ca(2+) exchanger. Five weeks after infarction, cardiac function was better maintained in TG than WT mice [left ventricular (LV) systolic pressure: WT, 41 +/- 2; TG, 58 +/- 3 mmHg; P < 0.05; maximum rising rate of LV pressure (+dP/dt(max)): WT, 3,750 +/- 346; TG, 5,075 +/- 334 mmHg/s; P < 0.05]. The isometric contractile response to beta-adrenergic stimulation was greater in papillary muscles from TG than WT mice (WT, 13.2 +/- 0.9; TG, 16.3 +/- 1.0 mN/mm(2) at 10(-4) M isoproterenol). The sarcoplasmic reticulum (SR) Ca(2+) content investigated by rapid cooling contractures in papillary muscles was greater in TG than WT mouse hearts. We conclude that myocardial function is better preserved in TG mice 5 wk after infarction, which results from enhanced SR Ca(2+) content via overexpression of the Na(+)/Ca(2+) exchanger. |
