Related Experiment Video
Updated: Jul 10, 2026
Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes
Published on: September 24, 2013
Mitochondrial big conductance KCa channel and cardioprotection in infant rabbit heart
Yang Shi1, Ming Tao Jiang, Jidong Su
1Surgery-Division of Pediatric Surgery, Medical College of Wisconsin, Mikwaukee, WI 53226, USA. yangshi@mcw.edu
Insights
Chronic hypoxia protects infant rabbit hearts from ischemia. However, this cardioprotection does not involve the mitochondrial big conductance Ca(2+)-sensitive K channel (mitoBKCa).
Area of Science:
- Cardiovascular Physiology
- Mitochondrial Function
- Neonatal Cardiology
Background:
- Chronic hypoxia confers resistance to myocardial ischemia in infant hearts.
- The mitochondrial big conductance Ca(2+)-sensitive K channel (mitoBKCa) is protective in adult hearts, but its role in infants is unknown.
Purpose of the Study:
- To investigate the role of mitoBKCa in the cardioprotection observed in infant rabbit hearts subjected to chronic hypoxia and ischemia-reperfusion.
Main Methods:
- Infant rabbit hearts from normoxic or hypoxic conditions were perfused with a mitoBKCa opener (NS1619) or blocker (Paxilline) prior to ischemia and reperfusion.
- Infarct size and recovery of left ventricular developed pressure (LVDP) were measured.
Main Results:
- Hypoxic hearts exhibited reduced infarct size and improved LVDP recovery compared to normoxic hearts.
- NS1619 decreased infarct size and improved LVDP in normoxic hearts but had no effect on hypoxic hearts.
- Paxilline did not alter outcomes in either normoxic or hypoxic hearts.
Conclusions:
- Activation of mitoBKCa protects normoxic infant rabbit hearts against ischemia-reperfusion injury.
- Cardioprotection afforded by chronic hypoxia in infant rabbits does not appear to be mediated by the mitoBKCa.
Abstract:
Chronic hypoxia increases resistance to myocardial ischemia in infants. Activation of the mitochondrial big conductance Ca(2+) -sensitive K channel (mitoBKCa) has been shown to be protective in adult hearts; however, its role in infant hearts is unknown. Hearts from normoxic or hypoxic infant rabbits were perfused with a mitoKCa opener, NS1619, or blocker Paxilline before ischemia and reperfusion. Hypoxic hearts were more resistant to ischemia than normoxic hearts as manifested by a reduction in infarct size (9 +/- 5% versus 14 +/- 5%) and an increase in recovery of left ventricular developed pressure (LVDP) (69 +/- 7% versus 51 +/- 2%). NS1619 decreased infarct size in normoxic hearts from 14 +/- 5% to 10 +/- 5% and increased recovery of LVDP from 51 +/- 2% to 65 +/- 4%, but it had no effect on hypoxic hearts. Paxilline did not affect normoxic or hypoxic hearts. Activation of mitoBKCa protects normoxic infant rabbit hearts; however, cardioprotection by chronic hypoxia in infant rabbits does not appear involve mitoBKCa.
