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Delayed myocardial preconditioning by α1-adrenoceptors involves inhibition of apoptosis
Journal article   Open access   Peer reviewed

Delayed myocardial preconditioning by α1-adrenoceptors involves inhibition of apoptosis

Kourosh Baghelai, Laura J. Graham, Andrew S. Wechsler and Emma R. Jakoi
The Journal of thoracic and cardiovascular surgery, v 117(5), pp 980-986
1999
DOI: https://doi.org/10.1016/S0022-5223(99)70379-X
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1016/s0022-5223(99)70379-xView
Published, Version of Record (VoR)Open Access (Publisher-Specific),  Open
url
https://doi.org/10.1016/S0022-5223(99)70379-XView
Published, Version of Record (VoR) Open

Abstract

Objective: Previous studies have demonstrated that α1-adrenoceptor activation increases myocardial resistance to ischemic injury 24 hours later. Here we tested the hypothesis that delayed protection is associated with limited infarction and involves altered expression of pro-apoptotic and/or anti-apoptotic proteins. Methods: Rabbits were treated with phenylephrine or an equivalent volume of vehicle (n = 6 per group). Twenty-four hours after pretreatment, isolated hearts were perfused with a bovine erythrocyte suspension in modified Krebs solution, subjected to 45 minutes of global ischemia (37°C), and reperfused for 120 minutes. Infarct size was determined by triphenyltetrazolium chloride staining. Apoptosis was quantified by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. Left ventricular tissue from separate groups of animals (n = 5 per group), 24 hours after pretreatment with phenylephrine or vehicle but without ischemia and reperfusion, was analyzed by Western blotting for content of the anti-apoptotic protein, bcl x, and pro-apoptotic protein, bax. Results: Isolated hearts after phenylephrine pretreatment had increased end-reperfusion developed pressures (56.8 ± 4.9 vs 36.2 ± 3.9 mm Hg for vehicle, P = .008) and decreased elevated end-diastolic pressures (26.7 ± 4.5 vs 42.3 ± 5.0 mm Hg for vehicle, P = .04). Phenylephrine pretreatment abrogated infarction (9.9 ± 2.4% vs 42.6 ± 6.3% for vehicle, P = .002) and reduced the number of apoptotic nuclei (24 ± 4.8 vs 51 ± 4.6 for vehicle, P = .038). Analysis by Western blotting showed that the ratio of bcl x to bax protein increased in phenylephrine-pretreated hearts (2.65 ± 0.5 vs 1.0 ± 0.1 for vehicle, P = .008). Conclusion: Delayed myocardial protection to infarction mediated by α1-adrenoceptor activation involves an increased bcl x/bax ratio, thereby limiting apoptotic cell death. (J Thorac Cardiovasc Surg 1999;117:980-6)

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Collaboration types
Domestic collaboration
Web of Science research areas
Cardiac & Cardiovascular Systems
Respiratory System
Surgery
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