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Endothelial preservation may merit attention in surgical myocardial protection; leaves open the differential roles of EDNO and EDHF pathways.
During cardiac surgery, the heart is arrested and subject to ischaemia-reperfusion injury. 2. To protect the heart, cardioplegia is usually used to initially stop and then maintain the still condition of the heart, which not only facilitates the precise operation but, more importantly, minimizes the energy consumption of the heart during this period. 3. The ischaemia-reperfusion injury may involve both myocytes and coronary endothelium-smooth muscle and, therefore, the protection of the heart should also involve these two aspects. 4. Injury to the heart involves: (i) ischaemia-reperfusion injury to the myocytes and coronary circulation; and (ii) possible injury to the coronary circulation by cardioplegia due to its hyperkalaemic components. 5. Injury to the coronary circulation may involve both endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF) mechanisms. The EDNO mechanism is susceptible to ischaemia-reperfusion, whereas the EDHF mechanism may be altered by hyperkalaemic cardioplegia. 6. To further protect the heart, supplemental therapy for EDNO and optimizing the components of cardioplegia to restore the EDHF mechanism may be important.
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Guo‐Wei He (1999) studied this question.
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