Expression of active α(1B)-adrenergic receptors in the heart does not alleviate ischemia reperfusion injury

Xiao Ming Gao, Bing Hui Wang, Elizabeth Woodcock, Xiao Jun Du

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22 Citations (Scopus)


Ischemic preconditioning reduces infarct size and improves cardiac function ha various species, including mice. The mechanism for ischemic preconditioning protection is not entirely clear and activation of α(1B)-adrenergic receptors (AR) is believed to be involved. Transgenic mice expressing constitutively active mutant α(1B)-AR in the heart have enhanced α(1B)-AR activity and therefore can be used to test the role of α(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 α(1B)-AR activity by cardiac-specific expression of constitutively active mutant α(1B)-AR in mice does not mimic ischemic preconditioning to protect against ischemia-reperfusion injury. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)1679-1686
Number of pages8
JournalJournal of Molecular and Cellular Cardiology
Issue number9
Publication statusPublished - 1 Jan 2000
Externally publishedYes


  • Infarct size
  • Ischemia
  • Ischemic preconditioning
  • Reperfusion
  • Transgenic mice
  • α(1B)-Adrenergic receptor

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