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Coronary endothelial function in open heart surgery
1Cardiovascular Research Laboratory, Grantham Hospital, University of Hong Kong. gwhe@hkucc.hku.hk
Insights
Hyperkalaemic cardioplegia used in heart surgery damages coronary endothelium-dependent hyperpolarizing factor (EDHF) function. This impairment affects cardiac function post-surgery, necessitating research into new cardioplegia solutions.
Area of Science:
- Cardiovascular Science
- Surgical Research
- Endothelial Biology
Background:
- Open heart surgery utilizes hyperkalaemic cardioplegia to arrest and protect the heart.
- Coronary endothelium may be damaged by ischemia-reperfusion and cardioplegia, impacting post-operative cardiac function.
- This damage can lead to increased mortality and morbidity after cardiac surgery.
Purpose of the Study:
- To investigate the effects of hyperkalaemia on coronary endothelial function.
- To assess the impact of varying potassium (K+) concentrations on endothelium-dependent relaxation and hyperpolarization.
- To determine if hyperkalaemia alters intracellular free calcium concentration in endothelial cells.
Main Methods:
- Studied coronary endothelial function following exposure to hyperkalaemia (20 or 50 mmol/L K+).
- Measured endothelium-dependent relaxation and hyperpolarization of coronary smooth muscle.
- Assessed intracellular free calcium concentration in endothelial cells in response to K+ exposure.
Main Results:
- Exposure to 20 or 50 mmol/L K+ significantly reduced endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation.
- Hyperpolarization of the membrane potential in response to endothelium-derived relaxing factor (EDRF) stimuli was also diminished by K+ exposure.
- Intracellular free calcium concentration in endothelial cells remained unchanged after hyperkalaemia exposure.
Conclusions:
- Hyperkalaemic cardioplegia impairs EDHF-mediated coronary endothelial function.
- The impairment results from altered EDHF effects on smooth muscle cells, likely affecting membrane potential and K+ channels, not biosynthesis or release.
- Development of new cardioplegia agents that preserve endothelial function during surgery is warranted.
Abstract:
1. During open heart surgery, the heart is arrested and protected by hyperkalaemic cardioplegia. The coronary endothelium may be damaged by ischaemia-reperfusion and cardioplegia. Subsequently, this may affect cardiac function immediately after cardiac surgery and cause mortality or morbidity. 2. Our studies have investigated coronary endothelial function after exposure to hyperkalaemia (K+ 20 or 50 mmol/L). Endothelium-dependent relaxation and hyperpolarization of the coronary smooth muscle and intracellular free calcium concentration in the endothelial cell were measured with regard to K+ exposure. 3. Endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation to A23187, bradykinin, and substance P in the presence of either U46619 (10 nmol/L)- or K+ (25 mmol/L)-induced contraction was reduced after exposure to either 20 or 50 mmol/L K+. 4. The hyperpolarization of the membrane potential in response to the endothelium-derived relaxing factor (EDRF) stimuli was also reduced by exposure to K+. 5. The intracellular free calcium concentration remained unchanged after exposure to hyperkalaemia. 6. We conclude that the EDHF-mediated coronary endothelial function is impaired after exposure to hyperkalaemic cardioplegia. The impairment of this function is due to the changed effect of EDHF on the smooth muscle cell, probably through partially depolarizing the membrane and affecting K+ channels rather than alteration of its biosynthesis/release in the endothelial cell. It may be of use to search for a new cardioplegia that preserves this endothelial function during open heart surgery.