title: Expression of active alpha(1B)-adrenergic receptors in the heart does not alleviate ischemic reperfusion injury.
abstract: 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.
authors.affiliation: Baker Medical Research Institute, Melbourne, Australia.
authors.forename: X M
authors.initials: XM
authors.lastname: Gao
authors.forename: B H
authors.initials: BH
authors.lastname: Wang
authors.forename: E
authors.initials: E
authors.lastname: Woodcock
authors.forename: X J
authors.initials: XJ
authors.lastname: Du
mesh_terms: D000818:Animals; D019194:Ischemic Preconditioning; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology*; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*
chemical_list: D018340:Receptors, Adrenergic, alpha-1