The role of adenosine in preconditioning by brief pressure overload in rats

Cheng Hsiung Huang, Shen Kou Tsai, Shu Chiung Chiang, Chang Chi Lai, Zen Chung Weng

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background/Purpose: Brief pressure overload of the left ventricle reduced myocardial infarct (MI) size in rabbits has been previously reported. Its effects in other species are not known. This study investigates effects of pressure overload and the role of adenosine in rats in this study. Methods: MI was induced by 40-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion. MI size was determined by triphenyl tetrazolium chloride staining. Brief pressure overload was induced by two 10-minute episodes of partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Results: The MI size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group as well as in the ischemic preconditioning group (17.4 ± 3.0% and 18.2 ± 1.5% vs. 26.6 ± 2.4% in the control group, p <0.001). Pretreatment with 8-(p-sulfophenyl)-theophylline (SPT), an inhibitor of adenosine receptors, did not significantly limit the protection by pressure overload and ischemic preconditioning (18.3 ± 1.5% and 18.2 ± 2.0%, respectively, p <0.001). SPT itself did not affect the extent of infarct (25.4 ± 2.0%). The hemodynamics, area at risk and mortality were not significantly different among all groups of animals. Conclusion: Brief pressure overload of the left ventricle preconditioned rat myocardium against infarction. Because SPT did not significantly alter MI size reduction, our results did not support a role of adenosine in preconditioning by pressure overload in rats.

Original languageEnglish
Pages (from-to)756-763
Number of pages8
JournalJournal of the Formosan Medical Association
Volume114
Issue number8
DOIs
Publication statusPublished - Aug 1 2015

Fingerprint

Adenosine
Pressure
Ischemic Preconditioning
Myocardial Infarction
Theophylline
Heart Ventricles
Coronary Vessels
Purinergic P1 Receptors
Coronary Occlusion
Ventricular Pressure
Infarction
Reperfusion
Aorta
Chlorides
Myocardium
Hemodynamics
Staining and Labeling
Rabbits
Control Groups
Mortality

Keywords

  • Adenosine
  • Ischemic preconditioning
  • Myocardial infarction
  • Pressure overload
  • Rats

ASJC Scopus subject areas

  • Medicine(all)

Cite this

The role of adenosine in preconditioning by brief pressure overload in rats. / Huang, Cheng Hsiung; Tsai, Shen Kou; Chiang, Shu Chiung; Lai, Chang Chi; Weng, Zen Chung.

In: Journal of the Formosan Medical Association, Vol. 114, No. 8, 01.08.2015, p. 756-763.

Research output: Contribution to journalArticle

Huang, Cheng Hsiung ; Tsai, Shen Kou ; Chiang, Shu Chiung ; Lai, Chang Chi ; Weng, Zen Chung. / The role of adenosine in preconditioning by brief pressure overload in rats. In: Journal of the Formosan Medical Association. 2015 ; Vol. 114, No. 8. pp. 756-763.
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abstract = "Background/Purpose: Brief pressure overload of the left ventricle reduced myocardial infarct (MI) size in rabbits has been previously reported. Its effects in other species are not known. This study investigates effects of pressure overload and the role of adenosine in rats in this study. Methods: MI was induced by 40-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion. MI size was determined by triphenyl tetrazolium chloride staining. Brief pressure overload was induced by two 10-minute episodes of partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50{\%} above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Results: The MI size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group as well as in the ischemic preconditioning group (17.4 ± 3.0{\%} and 18.2 ± 1.5{\%} vs. 26.6 ± 2.4{\%} in the control group, p <0.001). Pretreatment with 8-(p-sulfophenyl)-theophylline (SPT), an inhibitor of adenosine receptors, did not significantly limit the protection by pressure overload and ischemic preconditioning (18.3 ± 1.5{\%} and 18.2 ± 2.0{\%}, respectively, p <0.001). SPT itself did not affect the extent of infarct (25.4 ± 2.0{\%}). The hemodynamics, area at risk and mortality were not significantly different among all groups of animals. Conclusion: Brief pressure overload of the left ventricle preconditioned rat myocardium against infarction. Because SPT did not significantly alter MI size reduction, our results did not support a role of adenosine in preconditioning by pressure overload in rats.",
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AU - Tsai, Shen Kou

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N2 - Background/Purpose: Brief pressure overload of the left ventricle reduced myocardial infarct (MI) size in rabbits has been previously reported. Its effects in other species are not known. This study investigates effects of pressure overload and the role of adenosine in rats in this study. Methods: MI was induced by 40-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion. MI size was determined by triphenyl tetrazolium chloride staining. Brief pressure overload was induced by two 10-minute episodes of partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Results: The MI size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group as well as in the ischemic preconditioning group (17.4 ± 3.0% and 18.2 ± 1.5% vs. 26.6 ± 2.4% in the control group, p <0.001). Pretreatment with 8-(p-sulfophenyl)-theophylline (SPT), an inhibitor of adenosine receptors, did not significantly limit the protection by pressure overload and ischemic preconditioning (18.3 ± 1.5% and 18.2 ± 2.0%, respectively, p <0.001). SPT itself did not affect the extent of infarct (25.4 ± 2.0%). The hemodynamics, area at risk and mortality were not significantly different among all groups of animals. Conclusion: Brief pressure overload of the left ventricle preconditioned rat myocardium against infarction. Because SPT did not significantly alter MI size reduction, our results did not support a role of adenosine in preconditioning by pressure overload in rats.

AB - Background/Purpose: Brief pressure overload of the left ventricle reduced myocardial infarct (MI) size in rabbits has been previously reported. Its effects in other species are not known. This study investigates effects of pressure overload and the role of adenosine in rats in this study. Methods: MI was induced by 40-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion. MI size was determined by triphenyl tetrazolium chloride staining. Brief pressure overload was induced by two 10-minute episodes of partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Results: The MI size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group as well as in the ischemic preconditioning group (17.4 ± 3.0% and 18.2 ± 1.5% vs. 26.6 ± 2.4% in the control group, p <0.001). Pretreatment with 8-(p-sulfophenyl)-theophylline (SPT), an inhibitor of adenosine receptors, did not significantly limit the protection by pressure overload and ischemic preconditioning (18.3 ± 1.5% and 18.2 ± 2.0%, respectively, p <0.001). SPT itself did not affect the extent of infarct (25.4 ± 2.0%). The hemodynamics, area at risk and mortality were not significantly different among all groups of animals. Conclusion: Brief pressure overload of the left ventricle preconditioned rat myocardium against infarction. Because SPT did not significantly alter MI size reduction, our results did not support a role of adenosine in preconditioning by pressure overload in rats.

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