Superiority of hyperpolarizing to depolarizing cardioplegia in protection of coronary endothelial function Guo-Wei He, MD, PhD, Cheng-Qin Yang, MD The.

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Presentation transcript:

Superiority of hyperpolarizing to depolarizing cardioplegia in protection of coronary endothelial function Guo-Wei He, MD, PhD, Cheng-Qin Yang, MD The Journal of Thoracic and Cardiovascular Surgery Volume 114, Issue 4, Pages 643-650 (October 1997) DOI: 10.1016/S0022-5223(97)70055-2 Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 1 Coronary vascular tone during exposure to depolarization (potassium 20 mmol/L, K20) and hyperpolarization (aprikalim 100 μmol/L, APK –4). The depolarizing cardioplegic solution significantly contracted the coronary artery, but the hyperpolarizing solution relaxed the artery. n = 8 in each group. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 643-650DOI: (10.1016/S0022-5223(97)70055-2) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 2 Mean concentration (–log M)–relaxation (percentage of contraction by U46619 30 nmol/L) curves for EDHF-mediated relaxation induced by A23187 in the coronary arteries exposed to depolarization (potassium 20 mmol/L [K20], A) or hyperpolarization (aprikalim 100 μmol/L [APK –4], B) for 1 hour. The experiments were performed in the presence of indomethacin (7 μmol/L), a cyclooxygenase inhibitor, and l-NNA (300 μmol/L), a nitric oxide biosynthesis/release inhibitor. n = 8 in each group. E-, Endothelium-denuded arteries (n = 4). **p < 0.01. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 643-650DOI: (10.1016/S0022-5223(97)70055-2) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 2 Mean concentration (–log M)–relaxation (percentage of contraction by U46619 30 nmol/L) curves for EDHF-mediated relaxation induced by A23187 in the coronary arteries exposed to depolarization (potassium 20 mmol/L [K20], A) or hyperpolarization (aprikalim 100 μmol/L [APK –4], B) for 1 hour. The experiments were performed in the presence of indomethacin (7 μmol/L), a cyclooxygenase inhibitor, and l-NNA (300 μmol/L), a nitric oxide biosynthesis/release inhibitor. n = 8 in each group. E-, Endothelium-denuded arteries (n = 4). **p < 0.01. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 643-650DOI: (10.1016/S0022-5223(97)70055-2) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 3 Mean concentration (–log M)–relaxation (percentage of contraction by U46619 30 nmol/L) curves for EDHF-mediated relaxation induced by bradykinin in the coronary arteries exposed to depolarization (potassium 50 mmol/L [K50], n = 7 vs n = 13 in the control group; A) or hyperpolarization (aprikalim 100 μmol/L, APK −4, n = 7 vs n = 7 in the control group; B) for 1 hour. The experiments were performed in the presence of indomethacin (7 μmol/L) and l-NNA, 300 μmol/L. E-, Endothelium-denuded arteries (n = 4). *p < 0.05. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 643-650DOI: (10.1016/S0022-5223(97)70055-2) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 3 Mean concentration (–log M)–relaxation (percentage of contraction by U46619 30 nmol/L) curves for EDHF-mediated relaxation induced by bradykinin in the coronary arteries exposed to depolarization (potassium 50 mmol/L [K50], n = 7 vs n = 13 in the control group; A) or hyperpolarization (aprikalim 100 μmol/L, APK −4, n = 7 vs n = 7 in the control group; B) for 1 hour. The experiments were performed in the presence of indomethacin (7 μmol/L) and l-NNA, 300 μmol/L. E-, Endothelium-denuded arteries (n = 4). *p < 0.05. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 643-650DOI: (10.1016/S0022-5223(97)70055-2) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 4 Schematic diagram describing the possible pathway by which depolarizing (hyperkalemia) and hyperpolarizing (aprikalim) may affect the interaction between endothelium and smooth muscle. In response to the increase of the intracellular (cytosolic free) calcium level, endothelial cells derive three major EDRFs (PGI2, EDNO, and EDHF). These EDRFs decrease the intracellular calcium concentration in the smooth muscle cell through different mechanisms and ultimately relax the smooth muscle cell. The mechanism of EDHF to relax vessels is to open potassium channels and hyperpolarize the membrane. Subsequently, the voltage-operated calcium (Ca2+) channels are inhibited and therefore the calcium influx is reduced, and this causes relaxation. Use of hyperpolarizing cardioplegia may enhance this function because both potassium-channel openers (KCO) and EDHF relax the vessel by hyperpolarizing the membrane. In contrast, exposure to depolarizing cardioplegia (hyperkalemia) reduces the EDHF-mediated relaxation by affecting potassium channels and prolonged depolarization. The Journal of Thoracic and Cardiovascular Surgery 1997 114, 643-650DOI: (10.1016/S0022-5223(97)70055-2) Copyright © 1997 Mosby, Inc. Terms and Conditions