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Cardioplegia alters porcine coronary endothelial cell growth and responses to aggregating platelets
F N Nilsson1, V M Miller, C M Johnson
1Department of Surgery, Mayo Clinic, Rochester, Minn 55902.
Insights
Crystalloid cardioplegia used in heart transplantation impairs endothelial cell function and replication. This affects coronary artery responses to platelet products, potentially impacting transplant outcomes.
Area of Science:
- Cardiovascular Science
- Transplantation Biology
- Endothelial Cell Biology
Background:
- Cardioplegic solutions are crucial for preserving organs during cardiac transplantation.
- Endothelial cells play a vital role in vascular function and regulation.
- The impact of cardioplegia on endothelial cell response to platelet-derived factors is not fully understood.
Purpose of the Study:
- To investigate the effects of cardioplegic solutions on endothelial cell viability and function.
- To assess coronary artery responses to aggregating platelet products after cardioplegia.
- To evaluate the impact of crystalloid versus blood cardioplegia on endothelial cell replication.
Main Methods:
- Porcine coronary arteries were perfused with crystalloid or blood cardioplegic solutions.
- Isometric force measurements were performed on arterial rings with and without endothelium.
- Endothelial cell culture and scanning electron microscopy were utilized.
Main Results:
- Crystalloid cardioplegia reduced endothelium-dependent relaxations to platelet products immediately post-perfusion.
- These relaxations recovered after 5-hour storage, but endothelial cell replication was significantly reduced.
- Scanning electron microscopy revealed no anatomical differences in coronary arteries.
Conclusions:
- Crystalloid cardioplegia alters coronary artery responses to platelet-derived substances.
- The ability of endothelial cells to replicate is diminished following crystalloid cardioplegia.
- These findings suggest potential mechanisms for altered vascular resistance and structural changes in transplanted hearts.
Abstract:
Experiments were designed to determine the viability of endothelial cells and their responses to products released by aggregating platelets following single flush perfusion of the coronary arteries with cardioplegic solutions used for cardiac transplantation. Porcine coronary arteries were perfused with crystalloid (Plegisol) or blood cardioplegic solutions; nonperfused hearts placed in 0.9% saline were used as controls. Immediately following perfusion and after 5-hour storage of the hearts in the same cardioplegic solution, rings were cut from the right coronary arteries and suspended in organ chambers for the measurement of isometric force. In some rings the endothelium was removed deliberately. The left circumflex coronary arteries were flushed with collagenase and the harvested endothelial cells were plated for cell culture. Left anterior descending coronary arteries were perfusion fixed with glutaraldehyde for scanning electron microscopy. In the organ chamber experiments, aggregating platelets and adenosine diphosphate caused relaxations in rings with endothelium. These relaxations were reduced immediately following crystalloid cardioplegia and were restored following 5-hour storage. Serotonin caused contractions in all rings. Rings without endothelium were more sensitive than rings with endothelium to the amine; this difference was augmented following 5-hour storage of the heart. Significantly fewer foci of endothelial cells grew in culture following 5-hour storage of the hearts in crystalloid cardioplegic solution compared to control (p < 0.05). There were no anatomical differences identified among groups by scanning electron microscopy. These results suggest that crystalloid cardioplegia alters the responses of coronary arteries to substances released by aggregating platelets and reduces the ability of endothelial cells to replicate. Such changes may contribute to altered vascular resistance following reperfusion of transplanted hearts and potentially to later structural changes in the coronary arteries.