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GW24-e1805 Involvement of mitochondrial ATP-sensitive potassium channels and mitochondrial permeability transition pores in atorvastatin preconditioning-induced protection in isolated rat hearts
  1. Zhifang Zhao1,
  2. Yuanyuan Wang2,
  3. Xuze Li3,
  4. Haijuan Hu2,
  5. Wei Cui2
  1. 1Department of Respiration, The Third Hospital of Hebei Medical University, Shijiazhuang, China
  2. 2Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, China
  3. 3Department of Anesthesiology, The Second Hospital of Hebei Medical University, Shijiazhuang, China


Objectives To evaluate the cardioprotective effect of atorvastatin (Ator) via modulation of mitochondrial permeability transition pore (mPTP) through mitochondrial ATP-sensitive potassium channels (mitoKATP channels).

Methods Sprague-Dawley rat hearts were Langendorff-perfused with Krebs-Henseleit (K-H) buffer and subjected to 30 min global ischaemia followed by 120 min of reperfusion. In this study, the mitoKATP channels inhibitor 5-hydroxydecanoate (5-HD) and the mPTP opener lonidamine (LND) were used to analyse the underlying mechanisms. Rats were randomly divided into 7 groups: (1) control group; (2) ischaemia/reperfusion (I/R) group; (3) Ator group; (4) Ator + 5-HD group; (5)Ator + LND group; (6) 5-HD group; (7) LND group. The parameters of cardiac function, myocardial infarct size, lactate dehydrogenase (LDH) in the coronary effluent and ATP content in myocardium were measured. To investigate the relationship between mitoKATP channels and mPTP implicated in Ator preconditioning, NAD+ content, a marker of mPTP opening, was measured.

Results Compared with the I/R group, Ator (1 μM) preconditioning significantly improved cardiac functional recovery, decreased myocardial infarct size, reduced LDH release, prevented ATP and NAD+ depletion (P < 0.05 vs. I/R group). However, these protective effects of Ator were abolished in the presence of either 5-HD (100 μM) or LND (30 μM).

Conclusions Ator may protect myocardium in response to I/R injury by inhibiting the mPTP opening through activating the mitoKATP channels. Moreover, the mitoKATP channels may be upstream of the mPTP.

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