| First Author | Gao XM | Year | 2000 |
| Journal | J Mol Cell Cardiol | Volume | 32 |
| Issue | 9 | Pages | 1679-86 |
| PubMed ID | 10966830 | Mgi Jnum | J:127816 |
| Mgi Id | MGI:3765107 | Doi | 10.1006/jmcc.2000.1201 |
| Citation | Gao XM, et al. (2000) Expression of active alpha(1B)-adrenergic receptors in the heart does not alleviate ischemic reperfusion injury. J Mol Cell Cardiol 32(9):1679-86 |
| abstractText | Ischemic preconditioning reduces infarct size and improves cardiac function in various species, including mice. The mechanism for ischemic preconditioning protection is not entirely clear and activation of alpha(1B)-adrenergic receptors (AR) is believed to be involved. Transgenic mice expressing constitutively active mutant alpha(1B)-AR in the heart have enhanced alpha(1B)-AR activity and therefore can be used to test the role of alpha(1B)-AR in ischemic preconditioning. Wild-type and transgenic mice were subjected to 30- or 40-min periods of left coronary artery occlusion followed by 60-min reperfusion, or ischemic preconditioning prior to sustained ischemia-reperfusion. Risk and infarct zones were determined by staining with Evans blue and triphenyltetrazolium, respectively, and quantitated digitally. Infarct zone and infarct size were not different between wild-type and transgenic mice, nor was the extent of reduction in infarct size by preconditioning ischemia (wild-type mice: 45+/-3 to 18+/-3%, transgenic mice: 46+/-3 to 19+/-2% of the left ventricle, both P<0.01). Ventricular function was similar between wild-type and transgenic mice with or without ischemia-reperfusion injury. In conclusion, enhanced alpha(1B)-AR activity by cardiac-specific expression of constitutively active mutant alpha(1B)-AR in mice does not mimic ischemic preconditioning to protect against ischemia-reperfusion injury. |
