Ann Thorac Surg 2000;70:882
© 2000 The Society of Thoracic Surgeons
Invited commentary
Invited Commentary
Guo-Wei He, MD, PhDa
a Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China,
e-mail: gwhe{at}cuhk.edu.hk
Invited commentary
Depolarizing cardioplegia has been a standard and effective method to arrest and protect the heart during open-heart surgery. With increasing knowledge about the vascular endothelial function, particularly the discovery of not only nitric oxide (NO), but also other pathways such as so-called endothelium-derived hyperpolarizing factor (EDHF) has made the understanding on the physiology and pathophysiology of coronary circulation during cardioplegic arrest more complete. We have, in the recent years, reported the adverse effect of depolarizing cardioplegia on the EDHF-mediated pathway [1, 2]. Although the clinical role on this is still unclear because the strong effect of NO may well cover the effect of other factors, at least in critically ill patients, the complete protection of all functions of the coronary endothelium is beneficial to the perfusion of the myocardium and the recovery of the heart. One of the ways to protect the coronary endothelium is to use hyperpolarizing, rather than depolarizing cardioplegia [3]. The present study reports another possible method to protect the non-NO pathway, ie, using angiotensin converting enzyme (ACE) inhibitors to reduce the degradation of bradykinin and therefore to enhance the bradykinin-mediated endothelium-dependent relaxation. Although this is an interesting thinking and the experimental data are reliable, it is unknown what role bradykinin plays in the cardiac arrest period and perioperatively. In the laboratory setting, bradykinin is used as an "index" of endothelial function rather than as an important biological messenger, per se. Therefore, future studies should be designed to investigate whether the ACE inhibitor may affect the endothelial function in other aspects. In view of protection of the endothelial function, it will be a long way from the present study to the possible clinical use.
References
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He G.-W., Yang C.-Q., Graier W.F., Yang J.-A. Hyperkalemia alters EDHF-mediated hyperpolarization and relaxation in coronary arteries. Am J Physiol 1996;271(Heart Circ. Physiol. 40):H760-H767.[Abstract/Free Full Text]
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He G.-W., Yang C.-Q., Yang J.-A. Depolarizing cardiac arrest and EDHF-mediated hyperpolarization and relaxation in coronary arteries. J Thoracic Cardiovasc Surg 1997;113:932-941.[Abstract/Free Full Text]
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He G.-W., Yang C.-Q. Superiority of hyperpolarizing to depolarizing cardioplegia on the EDHF-mediated relaxation. J Thoracic Cardiovasc Surg 1997;114:643-650.[Abstract/Free Full Text]
