The protective effect of St. Thomas cardioplegia enriched with zacopride on the isolated rat heart
Related Experiment Video
Updated: May 17, 2026
Using an Isolated Working Rat Heart Model to Test Donor Heart Preservation Strategies
Published on: October 4, 2024
Bei Wu1, Cun Long, Feilong Hei
1Department of Extracorporeal Circulation, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Insights
Zacopride-enriched St. Thomas cardioplegia significantly reduces myocardial injury and improves heart function recovery in a rat model. This cardiac protection is linked to faster arrest and reduced infarct size, offering a promising therapeutic strategy for ischemia-reperfusion injury.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Cellular Biology
Background:
- Inward rectifier potassium channel (I(K1)) activation protects myocardial cells by shortening action potential duration and reducing calcium overload.
- Zacopride is a selective I(K1) agonist known to suppress arrhythmias in rat hearts.
Purpose of the Study:
- To investigate the protective effects of St. Thomas (ST) cardioplegia augmented with Zacopride against ischemia-reperfusion injury in an isolated rat heart model.
Main Methods:
- Isolated Sprague-Dawley rat hearts were perfused with Krebs-Henseleit buffer.
- Hearts were treated with control buffer, ST cardioplegia, or ST cardioplegia with Zacopride.
- Cardiac function and biochemical markers were assessed after reperfusion.
Main Results:
- Hearts treated with Zacopride-enriched ST cardioplegia arrested significantly faster.
- Improved recovery of left ventricular developed pressure, ±dP/dtmax, heart rate, and coronary flow was observed.
- Reduced cardiac troponin I levels, infarct size, and increased superoxide dismutase were noted in the Zacopride group.
Conclusions:
- St. Thomas cardioplegia enriched with Zacopride demonstrates significant cardioprotective effects against ischemia-reperfusion injury.
- Zacopride enhances the protective capabilities of cardioplegia, offering a potential therapeutic advancement.
- This study supports Zacopride as a beneficial additive to cardioplegia for cardiac surgery.
Abstract:
The activation of the heart inward rectifier potassium channel (I(K1) ) can reduce the injury of myocardial cells by shortening the action potential duration and reducing intracellular calcium overload. Zacopride is a selective I(K1) agonist and suppresses triggered arrhythmias in rat hearts. This investigation studied the effects of St. Thomas (ST) cardioplegia enriched with Zacopride on the isolated rat heart model. Sprague-Dawley rat hearts were harvested and perfused for 20 minutes with 37°C Krebs-Henseleit (KH) buffer followed by 15 minute perfusion with 4°C calcium-free KH buffer in the Control group (Con, n = 8), ST cardioplegia in the ST group (ST, n = 8) and ST cardioplegia with Zacopride in the STZ group (STZ, n = 8). After 45 minutes of arresting, all hearts were reperfused with 37°C KH buffer for 60 minutes. Hearts in the STZ group arrested faster than the Con and ST groups (9.25 ± 2.38 s vs. 72.25 ± 8.1 s, 12.75 ± 2.87 s). The recovery of the left ventricular developed pressure, ± dP/dtmax, heart rate, and coronary flow in the STZ group is significantly better than the other two groups during reperfusion. Compared with the Con and ST groups, the STZ group showed significant decreases in the maximum carciac troponin I level (P < 0.05) and the infarct size (P < 0.05). The superoxide dismutase level in the STZ group increased during the first 20 minutes of reperfusion (P < 0.05). ST cardioplegia enriched with Zacopride has beneficial effects against ischemia-reperfusion injury in this isolated rat heart model.
