Related Experiment Video
Updated: Oct 5, 2025
Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine
Published on: July 7, 2016
del Nido cardioplegia better preserves cardiac diastolic function but histidine-tryptophan-ketoglutarate is better
Hong-Mei Xue1,2,3, Hai-Tao Hou1, Wen-Tao Sun1,2
1The Institute of Cardiovascular Diseases & Department of Cardiovascular Surgery, TEDA International Cardiovascular Hospital, Tianjin University & Chinese Academy of Medical Sciences, Tianjin, China.
Insights
Comparing del Nido cardioplegia (DNC), histidine-tryptophan-ketoglutarate (HTK), and blood cardioplegia (BC) + HTK in a rat model, all protected against ischemia/reperfusion injury. DNC improved diastolic function, while HTK and BC + HTK better preserved endothelial function.
Area of Science:
- Cardiology
- Cardiovascular Surgery
- Biomedical Engineering
Background:
- Myocardial protection during cardiac surgery is critical.
- The optimal cardioplegia solution remains debated.
- Comparing del Nido cardioplegia (DNC), histidine-tryptophan-ketoglutarate (HTK), and blood cardioplegia (BC) + HTK is essential for clinical practice.
Purpose of the Study:
- To compare the cardiac and endothelial protection of DNC, HTK, and BC + HTK.
- To evaluate the efficacy of these cardioplegias in a rat model of ischemia/reperfusion (I/R).
Main Methods:
- Sixty male Wistar rats underwent 120 minutes of global ischemia and 90 minutes of reperfusion.
- Rats were randomly assigned to control, I/R, DNC, HTK, or BC + HTK groups.
- Hemodynamics, endothelium-dependent relaxation, and cardiac biomarkers (cTnT, CK-MB) were assessed.
Main Results:
- All three cardioplegias prevented myocardial damage from I/R injury.
- DNC showed better preserved left ventricular diastolic function.
- HTK and BC + HTK demonstrated superior preservation of endothelium-dependent relaxation.
Conclusions:
- No single cardioplegia currently offers 'perfect' protection.
- DNC excels in diastolic function preservation.
- HTK and BC + HTK are superior for maintaining coronary endothelial function.
- Further research is needed to develop an optimal cardioplegia solution.
Objectives:
The effectiveness of myocardial protection of cardioplegia has been a matter of debate for decades. This study was designed to compare cardiac and endothelial protection of 3 clinically used cardioplegias: del Nido cardioplegia (DNC), histidine-tryptophan-ketoglutarate (HTK) and blood cardioplegia (BC) followed by HTK (BC + HTK) in a rat model of ischaemia/reperfusion (I/R).
Methods:
Sixty male Wistar rats were subjected to either 120 min of global ischaemia at 4°C followed by 90 min of reperfusion (I/R) at 37°C or no I/R (control) in a Langendorff apparatus and were randomly allocated to 5 groups: control, I/R, DNC, HTK and BC + HTK. Cold cardioplegia solutions were administered at doses of 20 ml/kg for DNC and HTK or 10 ml/kg for BC followed by HTK. Haemodynamic parameters were continuously recorded using an intraventricular balloon. The endothelium-dependent relaxation to acetylcholine was measured in the left anterior descending artery using a myograph. Protein expression of cardiac troponin T (cTnT) and creatine kinase MB was determined by western blot.
Results:
During reperfusion, HTK had higher left ventricular systolic pressure whereas DNC had lower left ventricular end-diastolic pressure, better left ventricular developed pressure and best +dp/dtmax and -dp/dtmax than the other 2 groups but the differences disappeared at the end of the reperfusion. HTK or BC + HTK preserves the acetylcholine-induced endothelium-dependent relaxation better than DNC (Emax = 48.2 ± 8.0% in DNC vs 75.0 ± 8.0% in HTK, P < 0.05; vs 96.9 ± 3.5% in BC + HTK, P < 0.001). The protein levels of cTnT and creatine kinase MB were downregulated in the 3 groups.
Conclusions:
All 3 cardioplegias prevented myocardial damage against I/R injury at the end of reperfusion. DNC demonstrated better preserved diastolic function of the left ventricle whereas HTK or BC + HTK showed better preserved coronary endothelial function. These findings may suggest that currently no 'perfect' cardioplegia exists and that exploration for the 'perfect' cardioplegia is needed.
Related Concept Videos
01:26Heart Failure Drugs: Inotropic Agents
01:30Cardiomyopathy II: Dilated Cardiomyopathy
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System