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Induction and Assessment of Ischemia-reperfusion Injury in Langendorff-perfused Rat Hearts

Induction and Assessment of Ischemia-reperfusion Injury in Langendorff-perfused Rat Hearts

Published on: July 27, 2015

Dexmedetomidine preconditioning attenuates ischemia/reperfusion injury in isolated rat hearts with endothelial

Liang He¹, Shuqing Hao², Yanqiong Wang²

¹Department of Anesthesiology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, 650032, China; Department of Anesthesiology, Yan'an Hospital of Kunming City, Kunming Medical University, Kunming, Yunnan Province, 650051, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie

|April 10, 2019

Abstract

Background And Purposes:

Dexmedetomidine preconditioning (DP) can mimic pharmacological preconditioning and induce cardiac protection. There are controversies on the roles of coronary endothelia in cardioprotection of dexmedetomidine. Herein, we tested the hypothesis that protection of dexmedetomidine is not endothelial dependent in heart against myocardial ischemia/reperfusion (I/R) injury.

Methods:

Langendorff-perfused rat hearts were pretreated by 60 mM of potassium to produce endothelial dysfunction (ED), then medicated with dexmedetomidine, and subsequently subjected to 30 min of global ischemia followed by 60 min of reperfusion. To investigate the cardioprotective effect of dexmedetomidine in heart with ED, isolated rat hearts were randomly divided into the following six groups: sham, I/R, DP, ED, ED + I/R, and ED + DP + I/R. Heart rates, left ventricular function, and coronary perfusion pressure were assessed for each heart. Infarct size was evaluated by triphenyltetrazolium chloride staining. High-sensitivity cardiac troponin T (hs-cTNT) of coronary flow perfusion was determined.

Results:

After the isolated hearts with pretreatment of 60 mM of potassium chloride, diastolic function of coronary endothelia in performance of response to histamine was significantly decreased (P < 0.05). DP attenuated I/R-induced infarct size of the left ventricle (P < 0.05) and decreased hs-cTNT (P < 0.05). Additionally, left ventricular developed pressure, +dp/dt_max, and -dp/dt_max were elevated in rat hearts pretreated with dexmedetomidine. Furthermore, dexmedetomidine-mediated cardiac protection against I/R injury was still remained in isolated hearts with coronary ED.

Conclusion:

Continuous perfusion of 60 mM of potassium for 10 min can produce coronary ED in isolated rat hearts. Dexmedetomidine maintains its protective function against I/R injury in heart with coronary ED. Myocardial protection of dexmedetomidine is non-endothelial function dependent in alleviating I/R injury.

Keywords:

Dexmedetomidine Ischemia/reperfusion Preconditioning hs-cTNT

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