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Updated: Aug 18, 2026
Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
Published on: March 12, 2013
Selective mitochondrial K(ATP) channel activation results in antiarrhythmic effect during experimental myocardial
Biswadeep Das1, Chayna Sarkar, K Sudhakar Karanth
1Department of Pharmacology, Kasturba Medical College, Manipal, Karnataka, 576119, India. mcoms@mos.com.np
Abstract:
We investigated the effects of administration of non-hypotensive doses of ATP-sensitive K+ channel (K(ATP)) openers (nicorandil and aprikalim), and a specific mitochondrial K(ATP) channel blocker (5-hydroxydecanoate) prior to and during coronary occlusion as well as prior to and during post-ischemic reperfusion on survival rate, ischemia/reperfusion-induced arrhythmias and myocardial infarct size in anesthetized albino rabbits. Arrhythmias were induced by reperfusion following a 20 min ligation of the left main coronary artery with a releaseable silk ligature. Early intervention by intravenous infusion of nicorandil (100 microg/kg bolus+10 microg/kg/min) or aprikalim (10 microg/kg bolus+0.1 microg/kg/min) just before and during ischemia increased survival rate (86% and 75% vs. 55% in the control group), significantly decreased the incidence and severity of life-threatening arrhythmias and myocardial infarct size. The antiarrhythmic and cardioprotective effects of both nicorandil and aprikalim were abolished by pretreating the rabbits with 5-hydroxydecanoate (5 mg/kg, i.v. bolus). In conclusion, intervention by intravenous administration of nicorandil and aprikalim (through the selective activation of mitochondrial K(ATP) channels) increased survival rate and exhibited antiarrhythmic and cardioprotective effects during coronary occlusion and reperfusion in anesthetized rabbits when administered prior to and during coronary occlusion.
Insights
Administering ATP-sensitive potassium channel (K(ATP)) openers like nicorandil and aprikalim before and during ischemia improved survival and reduced arrhythmias and infarct size in rabbits. These cardioprotective effects were blocked by a mitochondrial K(ATP) channel blocker.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cell Physiology
Background:
- Myocardial ischemia/reperfusion injury remains a critical clinical challenge.
- ATP-sensitive potassium channels (K(ATP)) play a role in cardioprotection.
- Mitochondrial K(ATP) channels are potential therapeutic targets for ischemic heart disease.
Purpose of the Study:
- To investigate the cardioprotective effects of K(ATP) channel openers (nicorandil, aprikalim) and a blocker (5-hydroxydecanoate) in a rabbit model of myocardial ischemia/reperfusion.
- To determine the role of mitochondrial K(ATP) channels in mediating these protective effects.
Main Methods:
- Anesthetized rabbits underwent 20-minute coronary artery ligation followed by reperfusion.
- K(ATP) channel openers or blockers were administered intravenously before and during ischemia/reperfusion.
- Survival rate, incidence/severity of arrhythmias, and myocardial infarct size were assessed.
Main Results:
- Nicorandil and aprikalim significantly increased survival rates (86%, 75% vs. 55% in controls).
- Both drugs markedly reduced life-threatening arrhythmias and myocardial infarct size.
- Pretreatment with 5-hydroxydecanoate abolished the antiarrhythmic and cardioprotective effects of nicorandil and aprikalim.
Conclusions:
- Early intervention with K(ATP) channel openers, particularly through mitochondrial K(ATP) channel activation, enhances survival and provides antiarrhythmic and cardioprotective benefits during myocardial ischemia and reperfusion.
- Mitochondrial K(ATP) channels are crucial mediators of the cardioprotective effects of nicorandil and aprikalim.
